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1

Chandra, Atanu, Aritra K. Ray, Uddalak Chakraborty, and Arkapravo Hati. "Gut Microbiota and Extraintestinal Disorders: Are They Interrelated?" Bengal Physician Journal 7, no. 1 (2020): 8–11. http://dx.doi.org/10.5005/jp-journals-10070-7012.

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ABSTRACT Normally in health, the commensal gut microbiota lives in a perfectly symbiotic relationship with the host. Initial bacterial colonization occurs through the maternal vaginal/fecal flora and oral feeding. When this symbiotic relationship is lost due to several factors, the condition is known as “dysbiosis.” Dysbiosis is associated with the pathogenesis of intestinal disorders, such as inflammatory bowel disease, irritable bowel syndrome (IBS), and coeliac disease, but recent studies have shown that it has also been implicated in extraintestinal disorders, such as allergy, asthma, cardiovascular disease, obesity, autoimmune diseases, inflammatory diseases, and some mental disorders and cancers. The proposed mechanism for the development of such disorders is disruption of the pivotal mutual relationship between the gut microbiome, the metabolic products produced by them, and the host immune response. In this review article, we would like to highlight the role of gut microbiota in the development of extraintestinal diseases. How to cite this article: Chandra A, Ray AK, Chakraborty U, et al. Gut Microbiota and Extraintestinal Disorders: Are They Interrelated? Bengal Physician Journal 2020;7(1):8–11.
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Sampsell, Kara, Desirée Hao, and Raylene A. Reimer. "The Gut Microbiota: A Potential Gateway to Improved Health Outcomes in Breast Cancer Treatment and Survivorship." International Journal of Molecular Sciences 21, no. 23 (December 3, 2020): 9239. http://dx.doi.org/10.3390/ijms21239239.

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Breast cancer is the most frequently diagnosed cancer in women worldwide. The disease and its treatments exert profound effects on an individual’s physical and mental health. There are many factors that impact an individual’s risk of developing breast cancer, their response to treatments, and their risk of recurrence. The community of microorganisms inhabiting the gastrointestinal tract, the gut microbiota, affects human health through metabolic, neural, and endocrine signaling, and immune activity. It is through these mechanisms that the gut microbiota appears to influence breast cancer risk, response to treatment, and recurrence. A disrupted gut microbiota or state of ‘dysbiosis’ can contribute to a biological environment associated with higher risk for cancer development as well as contribute to negative treatment side-effects. Many cancer treatments have been shown to shift the gut microbiota toward dysbiosis; however, the microbiota can also be positively manipulated through diet, prebiotic and probiotic supplementation, and exercise. The objective of this review is to provide an overview of the current understanding of the relationship between the gut microbiota and breast cancer and to highlight potential strategies for modulation of the gut microbiota that could lead to improved clinical outcomes and overall health in this population.
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Qu, Wan, Shuo Liu, Weijie Zhang, Huawei Zhu, Qian Tao, Hua Wang, and He Yan. "Impact of traditional Chinese medicine treatment on chronic unpredictable mild stress-induced depression-like behaviors: intestinal microbiota and gut microbiome function." Food & Function 10, no. 9 (2019): 5886–97. http://dx.doi.org/10.1039/c9fo00399a.

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Gut microbiota dysbiosis is a recognized contributing factor to many noncommunicable diseases, but more evidence is still needed to illustrate its causative impact on mental and brain health disorders and mechanism(s) for targeted mitigation.
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Ericsson, Aaron. "355 The Gut Microbiome and its Influence on Cognition and Mental Health: from Zebrafish to Horses." Journal of Animal Science 98, Supplement_4 (November 3, 2020): 92–93. http://dx.doi.org/10.1093/jas/skaa278.169.

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Abstract The microbial communities colonizing the gastrointestinal tract of vertebrate hosts exist in symbiosis with their host, providing a wide array of functions that confer benefit to the collective superorganism. Intuitively, disruptions in microbial community structure can lead to deleterious host effects, and multiple associations have been made between gut inflammatory conditions and dysbiosis. Considering the myriad mechanisms of bi-directional communication between the gut microbiota and host autonomic nervous system, it is not surprising that the gut microbiota is now implicated as a factor in several behavioral, cognitive, and neuro-psychological conditions affecting people. While gut microbiomes have co-evolved with (and are very specific for) their cognate hosts, the functions provided by the communities are highly conserved, suggesting that the same microbiome-induced effects observed in people may also affect companion animals like horses. This presentation will show data generated in a range of host species including zebrafish, rodents, and horses, demonstrating the influence of the gut-brain axis on behavior, and physical and mental health. The objective is to provide listeners a new appreciation for the physiological, and perhaps clinical, influence of the gut microbiota, and implications for clinical practices such as antibiotic usage and feeding changes.
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Sonali, Sharma, Bipul Ray, Hediyal Ahmed Tousif, Annan Gopinath Rathipriya, Tuladhar Sunanda, Arehally M. Mahalakshmi, Wiramon Rungratanawanich, et al. "Mechanistic Insights into the Link between Gut Dysbiosis and Major Depression: An Extensive Review." Cells 11, no. 8 (April 16, 2022): 1362. http://dx.doi.org/10.3390/cells11081362.

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Depression is a highly common mental disorder, which is often multifactorial with sex, genetic, environmental, and/or psychological causes. Recent advancements in biomedical research have demonstrated a clear correlation between gut dysbiosis (GD) or gut microbial dysbiosis and the development of anxiety or depressive behaviors. The gut microbiome communicates with the brain through the neural, immune, and metabolic pathways, either directly (via vagal nerves) or indirectly (via gut- and microbial-derived metabolites as well as gut hormones and endocrine peptides, including peptide YY, pancreatic polypeptide, neuropeptide Y, cholecystokinin, corticotropin-releasing factor, glucagon-like peptide, oxytocin, and ghrelin). Maintaining healthy gut microbiota (GM) is now being recognized as important for brain health through the use of probiotics, prebiotics, synbiotics, fecal microbial transplantation (FMT), etc. A few approaches exert antidepressant effects via restoring GM and hypothalamus–pituitary–adrenal (HPA) axis functions. In this review, we have summarized the etiopathogenic link between gut dysbiosis and depression with preclinical and clinical evidence. In addition, we have collated information on the recent therapies and supplements, such as probiotics, prebiotics, short-chain fatty acids, and vitamin B12, omega-3 fatty acids, etc., which target the gut–brain axis (GBA) for the effective management of depressive behavior and anxiety.
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Chen, Yi-huan, Fen Xue, Shou-fen Yu, Xiao-sa Li, Ling Liu, Yan-yan Jia, Wen-jun Yan, Qing-rong Tan, Hua-ning Wang, and Zheng-wu Peng. "Gut microbiota dysbiosis in depressed women: The association of symptom severity and microbiota function." Journal of Affective Disorders 282 (March 2021): 391–400. http://dx.doi.org/10.1016/j.jad.2020.12.143.

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7

Trigo, M. "The role of the gut-brain axis in depression and anxiety disorders." European Psychiatry 64, S1 (April 2021): S695. http://dx.doi.org/10.1192/j.eurpsy.2021.1840.

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IntroductionThere is a bi-directional biochemical communication pathway between the gastrointestinal tract and the central nervous system, referred to as the “gut–brain axis”. Studies show that bacteria in the gastrointestinal tract, including commensal, probiotic, or pathogenic, can affect brain’s function. Since there is a symbiotic relationship between gut microbiota and the brain, changes in its composition can lead to dysbiosis, which plays a role in many psychiatric disorders, such as depression and anxiety, and therefore becomes a potential therapeutic target.ObjectivesTo examine data from recent studies regarding the gut-brain axis and its relationship with psychiatric disorders, such as depression and anxiety.MethodsReview of the most recent literature regarding the gut-brain axis and its relationship with depression and anxiety disorders. The research was carried out through the MedLine, PubMed, UptoDate, ScienceDirect, SciELO and SpringerLink databases, using the terms “gut-brain axis”, “depression” and “anxiety”, until December 2020.Results There is a relationship between dysbiosis of microbiota and some psychiatric disorders, particularly depression. Symbiosis may be restored by purposefully manipulate the gut microbiota using therapies such as probiotics, therefore enhancing beneficial bacteria in the gastrointestinal tract and improving symptoms of depression.ConclusionsAlthough probiotics can be used in the treatment of depression, further research is needed in order to carefully determine parameters such as the duration of treatment, dosage and drug interactions. Nonetheless, a better understanding of the gut-brain axis may arise new approaches on how we prevent and treat mental illnesses.DisclosureNo significant relationships.
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Jones, Lucas, Jessica Kumar, Adil Mistry, Thriveen Sankar Chittoor Mana, George Perry, V. Prakash Reddy, and Mark Obrenovich. "The Transformative Possibilities of the Microbiota and Mycobiota for Health, Disease, Aging, and Technological Innovation." Biomedicines 7, no. 2 (March 28, 2019): 24. http://dx.doi.org/10.3390/biomedicines7020024.

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The gut microbiota is extremely important for the health of the host across its lifespan.Recent studies have elucidated connections between the gut microbiota and neurological diseaseand disorders such as depression, anxiety, Alzheimer’s disease (AD), autism, and a host of otherbrain illnesses. Dysbiosis of the normal gut flora can have negative consequences for humans,especially throughout key periods during our lifespan as the gut microbes change with age in bothphenotype and number of bacterial species. Neurologic diseases, mental disorders, and euthymicstates are influenced by alterations in the metabolites produced by gut microbial milieu. Weintroduce a new concept, namely, the mycobiota and microbiota-gut-brain neuroendocrine axis anddiscuss co-metabolism with emphasis on means to influence or correct disruptions to normal gutflora throughout the lifespan from early development to old age. These changes involveinflammation and involve the permeability of barriers, such as the intestine blood barrier, the blood–brain barrier, and others. The mycobiota and microbiota–gut–brain axis offer new research horizonsand represents a great potential target for new therapeutics, including approaches based aroundinflammatory disruptive process, genetically engineered drug delivery systems, diseased cellculling “kill switches”, phage-like therapies, medicinal chemistry, or microbial parabiosis to namea few.
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Zhao, Ya-Fei, Da-Neng Wei, and Yong Tang. "Gut Microbiota Regulate Astrocytic Functions in the Brain: Possible Therapeutic Consequences." Current Neuropharmacology 19, no. 8 (August 11, 2021): 1354–66. http://dx.doi.org/10.2174/1570159x19666210215123239.

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Astrocytes are essential for maintaining the homeostasis of the central nervous system (CNS). Astrocytic dysfunction has been implicated in the progression of several neurodegenerative and psychiatric diseases; however, a multitude of factors and signals influencing astrocytic activity have not been entirely elucidated. Astrocytes respond to local signals from the brain, but are also indirectly modulated by gut microbiota. Previous studies revealed that most of the CNS diseases triggered by astrocytic dysfunction are closely associated with the dysbiosis of gut microbiome. Emerging data from preclinical and clinical studies suggest that the maturation and functioning of astrocytes rely on gut microbiota, which plays a pivotal role in the decrease of astrocytic activation and may alleviate symptoms of brain diseases. Herein, we discuss the most recent advances concerning the complex connections between astrocytes and gut microbiota, which are involved in the immune, neurotransmission and neuroendocrine pathways. Deciphering these pathways will facilitate a better understanding of how perturbed gut microbiota contributes to the dysfunction of astrocytes and open therapeutic opportunities for the treatment of brain diseases.
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Li, Shan, Dongyu Hua, Qiaoyan Wang, Ling Yang, Xinlei Wang, Ailin Luo, and Chun Yang. "The Role of Bacteria and Its Derived Metabolites in Chronic Pain and Depression: Recent Findings and Research Progress." International Journal of Neuropsychopharmacology 23, no. 1 (November 24, 2019): 26–41. http://dx.doi.org/10.1093/ijnp/pyz061.

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Abstract Background Chronic pain is frequently comorbid with depression in clinical practice. Recently, alterations in gut microbiota and metabolites derived therefrom have been found to potentially contribute to abnormal behaviors and cognitive dysfunction via the “microbiota–gut–brain” axis. Methods PubMed was searched and we selected relevant studies before October 1, 2019. The search keyword string included “pain OR chronic pain” AND “gut microbiota OR metabolites”; “depression OR depressive disorder” AND “gut microbiota OR metabolites”. We also searched the reference lists of key articles manually. Results This review systematically summarized the recent evidence of gut microbiota and metabolites in chronic pain and depression in animal and human studies. The results showed the pathogenesis and therapeutics of chronic pain and depression might be partially due to gut microbiota dysbiosis. Importantly, bacteria-derived metabolites, including short-chain fatty acids, tryptophan-derived metabolites, and secondary bile acids, offer new insights into the potential linkage between key triggers in gut microbiota and potential mechanisms of depression. Conclusion Studying gut microbiota and its metabolites has contributed to the understanding of comorbidity of chronic pain and depression. Consequently, modulating dietary structures or supplementation of specific bacteria may be an available strategy for treating chronic pain and depression.
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11

Hemant S Kanhere, Yogesh U Rahangdale, Ankita S Bodele, Dipesh I Wadhwani, Abhilasha R Ghoshewar, and Shweta P Karande. "Neurological disorders associated with impaired gut microbiota." GSC Biological and Pharmaceutical Sciences 015, no. 02 (May 30, 2021): 029–39. http://dx.doi.org/10.30574/gscbps.2021.15.2.0121.

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A growing field of studies is focusing on the microbiota-gut-brain axis in order to better understand the bidirectional communication pathways between gut bacteria and the CNS. The pathophysiology of neurological disorders including Alzheimer's disease and autism has been attributed to dysregulation of gut-brain axis. Fecal microbiota transplantation is the method of transferring faeces from a healthy donor into the intestine of a recipient in order to restore the recipient's weakened intestinal flora. It's been used to treat a wide range of conditions, including recurrent Clostridium difficile infection and inflammatory bowel disease. Gut-brain psychology will aid studies on subjects such as character, memory and behaviour and will contribute to the advancement of general psychology as well as will add more light in the field of neuropsychology. Lactobacillus and Bifidobacterium, for example, are essential components of the gut microbiota. Oligosaccharides, unsaturated fatty acids, dietary fibers and polyphenols are the most popular prebiotics. Traditional fermented foods including yoghurt, natto and pickles help to balance the gut bacteria. The gut microbiota is shaped by a person's diet and gut-brain function is controlled by it. Different types of microbiota have different effects on the brain and actions through the microbiota–gut–brain axis. Via the microbiota-gut-brain axis, a healthy diet leads to a healthy gut microbiota and brain and mental health. Dysbiosis of the gut microbiota has been shown to trigger depression-like behaviours in GF mice. Proinflammatory mediators such as iNOS, ROS, COX2 and NF-B are released by microglia, resulting in neuroinflammation in Alzheimer's disease. It is becoming more widely recognized as a symptom of Autism Spectrum Disorder. The establishment of gut-brain psychology is expected to have a significant impact on psychology and related disciplines.
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Bell, Victoria, Jorge Ferrão, Lígia Pimentel, Manuela Pintado, and Tito Fernandes. "One Health, Fermented Foods, and Gut Microbiota." Foods 7, no. 12 (December 3, 2018): 195. http://dx.doi.org/10.3390/foods7120195.

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Changes in present-day society such as diets with more sugar, salt, and saturated fat, bad habits and unhealthy lifestyles contribute to the likelihood of the involvement of the microbiota in inflammatory diseases, which contribute to global epidemics of obesity, depression, and mental health concerns. The microbiota is presently one of the hottest areas of scientific and medical research, and exerts a marked influence on the host during homeostasis and disease. Fermented foods and beverages are generally defined as products made by microbial organisms and enzymatic conversions of major and minor food components. Further to the commonly-recognized effects of nutrition on the digestive health (e.g., dysbiosis) and well-being, there is now strong evidence for the impact of fermented foods and beverages (e.g., yoghurt, pickles, bread, kefir, beers, wines, mead), produced or preserved by the action of microorganisms, on general health, namely their significance on the gut microbiota balance and brain functionality. Fermented products require microorganisms, i.e., Saccharomyces yeasts and lactic acid bacteria, yielding alcohol and lactic acid. Ingestion of vibrant probiotics, especially those contained in fermented foods, is found to cause significant positive improvements in balancing intestinal permeability and barrier function. Our guts control and deal with every aspect of our health. How we digest our food and even the food sensitivities we have is linked with our mood, behavior, energy, weight, food cravings, hormone balance, immunity, and overall wellness. We highlight some impacts in this domain and debate calls for the convergence of interdisciplinary research fields from the United Nations’ initiative. Worldwide human and animal medicine are practiced separately; veterinary science and animal health are generally neither considered nor inserted within national or international Health discussions. The absence of a clear definition and subsequent vision for the future of One Health may act as a barrier to transdisciplinary collaboration. The point of this mini review is to highlight the role of fermented foods and beverages on gut microbiota and debate if the need for confluence of transdisciplinary fields of One Health is feasible and achievable, since they are managed by separate sectors with limited communication.
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Musleh-Vega, Samir, Jorge Ojeda, and Pia M. Vidal. "Gut Microbiota–Brain Axis as a Potential Modulator of Psychological Stress after Spinal Cord Injury." Biomedicines 10, no. 4 (April 4, 2022): 847. http://dx.doi.org/10.3390/biomedicines10040847.

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A growing body of evidence from preclinical and clinical studies has associated alterations of the gut microbiota–brain axis with the progression and development of a number of pathological conditions that also affect cognitive functions. Spinal cord injuries (SCIs) can be produced from traumatic and non-traumatic causes. It has been reported that SCIs are commonly associated with anxiety and depression-like symptoms, showing an incidence range between 11 and 30% after the injury. These psychological stress-related symptoms are associated with worse prognoses in SCIs and have been attributed to psychosocial stressors and losses of independence. Nevertheless, emotional and mental modifications after SCI could be related to changes in the volume of specific brain areas associated with information processing and emotions. Additionally, physiological modifications have been recognized as a predisposing factor for mental health depletion, including the development of gut dysbiosis. This condition of imbalance in microbiota composition has been shown to be associated with depression in clinical and pre-clinical models. Therefore, the understanding of the mechanisms underlying the relationship between SCIs, gut dysbiosis and psychological stress could contribute to the development of novel therapeutic strategies to improve SCI patients’ quality of life.
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Gallop, Amy, James Weagley, Saif-ur-Rahman Paracha, and George Grossberg. "The Role of The Gut Microbiome in Parkinson’s Disease." Journal of Geriatric Psychiatry and Neurology 34, no. 4 (July 2021): 253–62. http://dx.doi.org/10.1177/08919887211018268.

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The gut microbiota is known to play a role in various disease states through inflammatory, immune and endocrinologic response. Parkinson’s Disease is of particular interest as gastrointestinal involvement is one of the earlier features seen in this disease. This paper examines the relationship between gut microbiota and Parkinson’s Disease, which has a growing body of literature. Inflammation caused by gut dysbiosis is thought to increase a-synuclein aggregation and worsen motor and neurologic symptoms of Parkinson’s disease. We discuss potential treatment and supplementation to modify the microbiota. Some of these treatments require further research before recommendations can be made, such as cord blood transplant, antibiotic use, immunomodulation and fecal microbiota transplant. Other interventions, such as increasing dietary fiber, polyphenol and fermented food intake, can be made with few risks and may have some benefit for symptom relief and speed of disease progression.
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Jiang, Sha, Jia-Ying Hu, and Heng-Wei Cheng. "The Impact of Probiotic Bacillus subtilis on Injurious Behavior in Laying Hens." Animals 12, no. 7 (March 30, 2022): 870. http://dx.doi.org/10.3390/ani12070870.

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Intestinal microbiota functions such as an endocrine organ to regulate host physiological homeostasis and behavioral exhibition in stress responses via regulating the gut–brain axis in humans and other mammals. In humans, stress-induced dysbiosis of the gut microbiota leads to intestinal permeability, subsequently affecting the clinical course of neuropsychiatric disorders, increasing the frequency of aggression and related violent behaviors. Probiotics, as direct-fed microorganism, have been used as dietary supplements or functional foods to target gut microbiota (microbiome) for the prevention or therapeutic treatment of mental diseases including social stress-induced psychiatric disorders such as depression, anxiety, impulsivity, and schizophrenia. Similar function of the probiotics may present in laying hens due to the intestinal microbiota having a similar function between avian and mammals. In laying hens, some management practices such as hens reared in conventional cages or at a high stocking density may cause stress, leading to injurious behaviors such as aggressive pecking, severe feather pecking, and cannibalism, which is a critical issue facing the poultry industry due to negative effects on hen health and welfare with devastating economic consequences. We discuss the current development of using probiotic Bacillus subtilis to prevent or reduce injurious behavior in laying hens.
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Ghorbani, Mahin, Gerard Benedict, Tew Mei Mei, Muhamad Syahril bin Mod Yusub, Siti SalwaRamly, Muhamad Arif bin Muhamad Rasat, Stella Loke, et al. "T176. INSIGHTS INTO THE ROLE OF ORAL AND GUT MICROBIOME IN THE PATHOGENESIS OF SCHIZOPHRENIA." Schizophrenia Bulletin 46, Supplement_1 (April 2020): S298. http://dx.doi.org/10.1093/schbul/sbaa029.736.

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Abstract Background The role of oral and gut microbiomes in the pathogenesis of schizophrenia has recently come to light with the advancement of sequencing technology. Recent studies have shown that schizophrenia patients have different gut and oral microbiome profiles than healthy people. The interaction of oral and gut microbiota with the brain is facilitated through the gut-brain axis. Several studies have profiled the gut microbiomes in the Malaysian population, however none has investigated its relationship with etiology of schizophrenia. The aim of this preliminary study is to therefore investigate the relationship between oral and gut microbiomes in pathogenesis of schizophrenia in the Malaysian population based on the total transcriptome profiles. Methods In this study, 15 schizophrenia patients and 15 healthy people (control) were recruited from the three major ethnic groups in Malaysia, namely Malay, Chinese and Indian. Throat swabs and stool samples were collected and subjected to total RNA extraction. Following this, ribosomal RNA depletion and cDNA conversion were performed prior to sequencing using Illumina platform. Bioinformatic tools will be used to analyse and compare the transcriptome profiles of microbiomes from schizophrenia and healthy subjects. Brain derived neurotrophic factor, serotonin and dopamine assays will be performed using their blood samples too. The results of the bioassays will be then correlated with the transcriptome profiles to identify possible mechanisms by which microbiota could promote schizophrenia Results The RNA sequencing results will reveal differences in gene expression profiles between the microbiomes of schizophrenic and healthy subjects. Based on the transcriptome profiles and bioassay results, the possible pathways and mechanisms by which these microbiota can cause schizophrenia will be identified. In addition, candidate biomarkers from the oral and/or gut microbiomes for diagnosis of schizophrenia can be identified. Discussion The first and second generations of schizophrenia treatments mostly are based on controlling the symptoms of the disease, whereas treatment based on microbiome dysbiosis correction can tackle the underlying mechanism leading to a precise treatment of the disease.The findings from this study will enable the identification of distinct schizophrenia associated bacteria, that may help in development of new treatments and novel diagnostics for schizophrenia via microbiome-targeted therapy including probiotics and prebiotic.
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Kaur, Gagandeep, Tapan Behl, Simona Bungau, Arun Kumar, Md Sahab Uddin, Vineet Mehta, Gokhan Zengin, Bijo Mathew, Muhammad Ajmal Shah, and Sandeep Arora. "Dysregulation of the Gut-Brain Axis, Dysbiosis and Influence of Numerous Factors on Gut Microbiota Associated Parkinson’s Disease." Current Neuropharmacology 19, no. 2 (December 31, 2020): 233–47. http://dx.doi.org/10.2174/1570159x18666200606233050.

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Background: Parkinson’s disease (PD) has been one of the substantial social, medical concern and, burdens of the present time. PD is a gradually devastating neurodegenerative disorder of the neurological function marked with αsynucleinopathy affecting numerous regions of the brain-gut axis, as well as the central, enteric, and autonomic nervous system. Its etiology is a widely disputed topic. Objective: This review emphasizes to find out the correlation among the microbial composition and the observable disturbances in the metabolites of the microbial species and its impact on the immune response, which may have a concrete implication on the occurrence, persistence and, pathophysiology of PD via the gut-brain axis. Methods: An in-depth research and the database was developed from the available peer reviewed articles till date (March 2020) utilizing numerous search engines like PubMed, MEDLINE and, other internet sources. Results: Progressively increasing shreds of evidence have proved the fact that dysbiosis in the gut microbiome plays a central role in many neurological disorders, such as PD. Indeed, a disordered microbiome-gut-brain axis in PD could be focused on gastrointestinal afflictions that manifest primarily several years prior to the diagnosis, authenticating a concept wherein the pathological pathway progresses from the intestine reaching the brain. Conclusion: The microbiota greatly affects the bidirectional interaction between the brain and the gut via synchronized neurological, immunological, and neuroendocrine mechanisms. It can be concluded that a multitude of factors discussed in this review steadily induce the onset of dysbacteriosis that may exacerbate the etiologic mechanism of Parkinson’s disease.
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Ortega, Miguel A., Miguel Angel Alvarez-Mon, Cielo García-Montero, Oscar Fraile-Martinez, Luis G. Guijarro, Guillermo Lahera, Jorge Monserrat, et al. "Gut Microbiota Metabolites in Major Depressive Disorder—Deep Insights into Their Pathophysiological Role and Potential Translational Applications." Metabolites 12, no. 1 (January 8, 2022): 50. http://dx.doi.org/10.3390/metabo12010050.

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The gut microbiota is a complex and dynamic ecosystem essential for the proper functioning of the organism, affecting the health and disease status of the individuals. There is continuous and bidirectional communication between gut microbiota and the host, conforming to a unique entity known as “holobiont”. Among these crosstalk mechanisms, the gut microbiota synthesizes a broad spectrum of bioactive compounds or metabolites which exert pleiotropic effects on the human organism. Many of these microbial metabolites can cross the blood–brain barrier (BBB) or have significant effects on the brain, playing a key role in the so-called microbiota-gut-brain axis. An altered microbiota-gut-brain (MGB) axis is a major characteristic of many neuropsychiatric disorders, including major depressive disorder (MDD). Significative differences between gut eubiosis and dysbiosis in mental disorders like MDD with their different metabolite composition and concentrations are being discussed. In the present review, the main microbial metabolites (short-chain fatty acids -SCFAs-, bile acids, amino acids, tryptophan -trp- derivatives, and more), their signaling pathways and functions will be summarized to explain part of MDD pathophysiology. Conclusions from promising translational approaches related to microbial metabolome will be addressed in more depth to discuss their possible clinical value in the management of MDD patients.
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Lai, Zhongmeng, Weiran Shan, Jun Li, Jia Min, Xianzhang Zeng, and Zhiyi Zuo. "Appropriate exercise level attenuates gut dysbiosis and valeric acid increase to improve neuroplasticity and cognitive function after surgery in mice." Molecular Psychiatry 26, no. 12 (October 18, 2021): 7167–87. http://dx.doi.org/10.1038/s41380-021-01291-y.

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AbstractPostoperative cognitive dysfunction (POCD) affects the outcome of millions of patients each year. Aging is a risk factor for POCD. Here, we showed that surgery induced learning and memory dysfunction in adult mice. Transplantation of feces from surgery mice but not from control mice led to learning and memory impairment in non-surgery mice. Low intensity exercise improved learning and memory in surgery mice. Exercise attenuated surgery-induced neuroinflammation and decrease of gut microbiota diversity. These exercise effects were present in non-exercise mice receiving feces from exercise mice. Exercise reduced valeric acid, a gut microbiota product, in the blood. Valeric acid worsened neuroinflammation, learning and memory in exercise mice with surgery. The downstream effects of exercise included attenuating growth factor decrease, maintaining astrocytes in the A2 phenotypical form possibly via decreasing C3 signaling and improving neuroplasticity. Similar to these results from adult mice, exercise attenuated learning and memory impairment in old mice with surgery. Old mice receiving feces from old exercise mice had better learning and memory than those receiving control old mouse feces. Surgery increased blood valeric acid. Valeric acid blocked exercise effects on learning and memory in old surgery mice. Exercise stabilized gut microbiota, reduced neuroinflammation, attenuated growth factor decrease and preserved neuroplasticity in old mice with surgery. These results provide direct evidence that gut microbiota alteration contributes to POCD development. Valeric acid is a mediator for this effect and a potential target for brain health. Low intensity exercise stabilizes gut microbiota in the presence of insult, such as surgery.
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Minaya, Dulce M., Noah L. Weinstein, and Krzysztof Czaja. "Development of a 3D-Printed High Temperature Resin Cecal Fistula Implant for Long-Term and Minimally Invasive Access to the Gut Microbiome." Nutrients 13, no. 12 (December 17, 2021): 4515. http://dx.doi.org/10.3390/nu13124515.

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Microbiota dysbiosis has been associated with chronic diseases ranging from gastrointestinal inflammatory and metabolic conditions to neurological changes affecting the gut-brain neural axis, mental health, and general well-being. However, current animal studies using oral gavage and gnotobiotic animals do not allow for non-invasive long-term access to gut microbiome. The purpose of the present study was to evaluate the feasibility of 3D-printed fistula implants through the body wall and into the cecum of rats to obtain long-term access to gut microbiome. Cecal fistulas were designed and 3D-printed using a high temperature resin (Formlabs; acrylic and methacrylic mixture). Nine male Sprague-Dawley rats underwent the fistula implantation. Food intake, body weight, and body fat were measured to determine the impact of fistula manipulation. Gut microbiome, vagal afferents in the hindbrain, and microglia activation were analyzed to determine if fistula implantation disrupted the gut-brain neural axis. We found that the procedure induced a transient decrease in microbial diversity in the gut that resolved within a few weeks. Fistula implantation had no impact on food intake, body weight, fat mass, or microglia activation. Our study shows that 3D-printed cecal fistula implantation is an effective procedure that allows long-term and minimally invasive access to gut microbiome.
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De la Fuente, Mónica. "The Role of the Microbiota-Gut-Brain Axis in the Health and Illness Condition: A Focus on Alzheimer’s Disease." Journal of Alzheimer's Disease 81, no. 4 (June 15, 2021): 1345–60. http://dx.doi.org/10.3233/jad-201587.

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Trillions of commensal microbes live in our body, the majority in the gut. This gut microbiota is in constant interaction with the homeostatic systems, the nervous, immune and endocrine systems, being fundamental for their appropriate development and function as well as for the neuroimmunoendocrine communication. The health state of an individual is understood in the frame of this communication, in which the microbiota-gut-brain axis is a relevant example. This bidirectional axis is constituted in early age and is affected by many environmental and lifestyle factors such as diet and stress, among others, being involved in the adequate maintenance of homeostasis and consequently in the health of each subject and in his/her rate of aging. For this, an alteration of gut microbiota, as occurs in a dysbiosis, and the associated gut barrier deterioration and the inflammatory state, affecting the function of immune, endocrine and nervous systems, in gut and in all the locations, is in the base of a great number of pathologies as those that involve alterations in the brain functions. There is an age-related deterioration of microbiota and the homeostatic systems due to oxi-inflamm-aging, and thus the risk of aging associated pathologies such as the neurodegenerative illness. Currently, this microbiota-gut-brain axis has been considered to have a relevant role in the pathogenesis of Alzheimer’s disease and represents an important target in the prevention and slowdown of the development of this pathology. In this context, the use of probiotics seems to be a promising help.
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Yahfoufi, Nour, Chantal Matar, and Nafissa Ismail. "Adolescence and Aging: Impact of Adolescence Inflammatory Stress and Microbiota Alterations on Brain Development, Aging, and Neurodegeneration." Journals of Gerontology: Series A 75, no. 7 (January 10, 2020): 1251–57. http://dx.doi.org/10.1093/gerona/glaa006.

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Abstract Puberty/adolescence is a critical phase during neurodevelopment with numerous structural, neurochemical, and molecular changes occurring in response to genetic and environmental signals. A consequence of this major neuronal reorganizing and remodeling is a heightened level of vulnerability to stressors and immune challenges. The gut microbiota is a fundamental modulator of stress and immune responses and has been found to play a role in mental health conditions and neurodegenerative disorders. Environmental insults (stress, infection, neuroinflammation, and use of antibiotics) during adolescence can result in dysbiosis subsidizing the development of brain disorders later in life. Also, pubertal neuroinflammatory insults can alter neurodevelopment, impact brain functioning in an enduring manner, and contribute to neurological disorders related to brain aging, such as Alzheimer’s disease, Parkinson’s disease, and depression. Exposure to probiotics during puberty can mitigate inflammation, reverse dysbiosis, and decrease vulnerabilities to brain disorders later in life. The goal of this review is to reveal the consequences of pubertal exposure to stress and immune challenges on the gut microbiota, immune reactivity within the brain, and the risk or resilience to stress-induced mental illnesses and neurodegenerative disorders. We propose that the consumption of probiotics during adolescence contribute to the prevention of brain pathologies in adulthood.
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Ciocan, Dragos, Anne-Marie Cassard, Laurent Becquemont, Céline Verstuyft, Cosmin Sebastian Voican, Khalil El Asmar, Romain Colle, et al. "Blood microbiota and metabolomic signature of major depression before and after antidepressant treatment: a prospective case–control study." Journal of Psychiatry & Neuroscience 46, no. 3 (May 1, 2021): E358—E368. http://dx.doi.org/10.1503/jpn.200159.

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Background: The microbiota interacts with the brain through the gut–brain axis, and a distinct dysbiosis may lead to major depressive episodes. Bacteria can pass through the gut barrier and be found in the blood. Using a multiomic approach, we investigated whether a distinct blood microbiome and metabolome was associated with major depressive episodes, and how it was modulated by treatment. Methods: In this case–control multiomic study, we analyzed the blood microbiome composition, inferred bacterial functions and metabolomic profile of 56 patients experiencing a current major depressive episode and 56 matched healthy controls, before and after treatment, using 16S rDNA sequencing and liquid chromatography coupled to tandem mass spectrometry. Results: The baseline blood microbiome in patients with a major depressive episode was distinct from that of healthy controls (patients with a major depressive episode had a higher proportion of Janthinobacterium and lower levels of Neisseria) and changed after antidepressant treatment. Predicted microbiome functions confirmed by metabolomic profiling showed that patients who were experiencing a major depressive episode had alterations in the cyanoamino acid pathway at baseline. High baseline levels of Firmicutes and low proportions of Bosea and Tetrasphaera were associated with response to antidepressant treatment. Based on inferred baseline metagenomic profiles, bacterial pathways that were significantly associated with treatment response were related to xenobiotics, amino acids, and lipid and carbohydrate metabolism, including tryptophan and drug metabolism. Metabolomic analyses showed that plasma tryptophan levels are independently associated with response to antidepressant treatment. Limitations: Our study has some limitations, including a lack of information on blood microbiome origin and the lack of a validation cohort to confirm our results. Conclusion: Patients with depression have a distinct blood microbiome and metabolomic signature that changes after treatment. Dysbiosis could be a new therapeutic target and prognostic tool for the treatment of patients who are experiencing a major depressive episode.
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Ling, Yi, Qilu Gu, Junmei Zhang, Tianyu Gong, Xiongpeng Weng, Jiaming Liu, and Jing Sun. "Structural Change of Gut Microbiota in Patients with Post-Stroke Comorbid Cognitive Impairment and Depression and Its Correlation with Clinical Features." Journal of Alzheimer's Disease 77, no. 4 (October 13, 2020): 1595–608. http://dx.doi.org/10.3233/jad-200315.

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Background: Post-stroke comorbid cognitive impairment and depression (PSCCID) is a severe neuropsychiatric complication after acute stroke. Gut microbiota dysbiosis is associated with many psychiatric disorders. Alterations in the composition of gut microbiota may serve as a critical role in patients with PSCCID. Objective: We aimed to characterize the microbial profiles of patients with PSCCID. Method: A total of 175 stroke patients were recruited in the study. The composition of gut bacterial communities of patients was determined by 16S ribosomal RNA Miseq sequencing, and Phylogenetic Investigation of Communities by Reconstruction of Unobserved States was used to demonstrate the functional alterations of gut microbiota. We further identified the characteristic gut microbiota of PSCCID using linear discriminant analysis effect size. Results: Patients with PSCCID exhibited an increased abundance of Proteobacteria, including Gammaproteobacteria, Enterobacteriales, and Enterobacteriaceae, and a decreased abundance of several short-chain fatty acids-producing bacteria compared with non-PSCCID patients. The abundance of Gammaproteobacteria and Enterobacteriaceae showed negative correlations with the MoCA score. Moreover, the Kyoto Encyclopedia of Genes and Genomes results demonstrated the enriched orthologs of glycan biosynthesis and metabolism and decreased orthologs of amino acid metabolism in PSCCID patients. Importantly, the characteristic gut microbiota was identified and achieved an area under the curve of 0.847 between the two groups. Conclusion: In this study, we characterized the gut microbiota of PSCCID patients, and revealed the correlations of the altered gut microbiota with clinical parameters, which took a further step towards non-invasive diagnostic biomarkers for PSCCID from fecal samples.
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Lubomski, Michal, Ai Huey Tan, Shen-Yang Lim, Andrew Holmes, Ryan L. Davis, and Carolyn M. Sue. "082 The gastrointestinal microbiome in parkinson’s disease: impacts of motor and non-motor features, medications, lifestyle and diet." Journal of Neurology, Neurosurgery & Psychiatry 90, e7 (July 2019): A26.2—A26. http://dx.doi.org/10.1136/jnnp-2019-anzan.70.

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IntroductionThe human gastrointestinal microbiome (GM) has been proposed to be integral in the pathogenesis of Parkinson’s disease (PD). Evidence supports a bidirectional interaction between the brain and the gut that is mediated by the GM. Dysbiosis of the GM is believed to negatively influence vital physiological functions in many diseases.MethodsWe reviewed the literature on changes in human physiological function associated with gut microbial community states in PD. In particular, we evaluated the literature for effects of GM dysbiosis on motor and non-motor features, dietary and lifestyle factors and medication use in PD.ResultsAltered GM profiles in PD have been suggested to disrupt vital signalling pathways within the microbiota-gut-brain axis, integral to regulating physiological digestive function and metabolic homeostasis. Unfavourable variations in the GM have been shown to perturb mood (anxiety/depression), cognition, perception (hallucinations/delusions), gastrointestinal motility, including constipation in PD. Further, varied clinical motor phenotypes, including postural instability and gait disturbance have been attributed to alterations in the GM, in addition to the use of catechol-O-methyltransferase inhibitors, anticholinergics and levodopa. Variations in dietary and lifestyle factors have also been inferred to cause alterations in GM profiles, including caffeine consumption, macronutrient intake, smoking and the effects of ageing and exercise.ConclusionsIt is apparent from the mounting evidence that alterations in the GM are intimately involved in PD pathogenesis. However, the GM can also be modulated by dietary, lifestyle and treatment factors that may influence motor and non-motor features as well as disease progression.
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Gonzalez-Mercado, Velda J., Jean Lim, Leorey N. Saligan, Nicole Perez, Carmen Rodriguez, Raul Bernabe, Samia Ozorio, Elsa Pedro, Farrah Sepehri, and Brad Aouizerat. "Gut Microbiota and Depressive Symptoms at the End of CRT for Rectal Cancer: A Cross-Sectional Pilot Study." Depression Research and Treatment 2021 (December 29, 2021): 1–10. http://dx.doi.org/10.1155/2021/7967552.

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Background. The role of alterations in gut microbiota composition (termed dysbiosis) has been implicated in the pathobiology of depressive symptoms; however, evidence remains limited. This cross-sectional pilot study is aimed at exploring whether depressive symptom scores changed during neoadjuvant chemotherapy and radiation therapy to treat rectal cancer, and if gut microbial taxa abundances and predicted functional pathways correlate with depressive symptoms at the end of chemotherapy and radiation therapy. Methods. 40 newly diagnosed rectal cancer patients (ages 28-81; 23 males) were assessed for depressive symptoms using the Hamilton Rating Scale for Depression (HAM-D) and provided stool samples for 16S rRNA sequencing. Gut microbiome data were analyzed using QIIME2, and correlations and regression analyses were performed in R. Results. Participants had significantly higher depressive symptoms at the end as compared to before CRT. The relative abundances of Gemella, Bacillales Family XI, Actinomyces, Streptococcus, Lactococcus, Weissella, and Leuconostocaceae were positively correlated (Spearman’s rho = 0.42 to 0.32), while Coprobacter, Intestinibacter, Intestimonas, Lachnospiraceae, Phascolarctobacterium, Ruminiclostridium, Ruminococcaceae (UCG-005 and uncultured), Tyzzerella, and Parasutterella (Spearman’s rho = − 0.43 to − 0.31 ) were negatively correlated with HAM-D scores. Of the 14 predicted MetaCyc pathways that correlated with depressive symptom scores at the end of CRT, 11 (79%) were associated with biosynthetic pathways. Conclusions. Significant bacterial taxa and predicted functional pathways correlated with depressive symptoms at the end of chemotherapy and radiation therapy for rectal cancer which warrants further examination and replication of our findings.
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Elmaleh, David R., Matthew A. Downey, Ljiljana Kundakovic, Jeremy E. Wilkinson, Ziv Neeman, and Eran Segal. "New Approaches to Profile the Microbiome for Treatment of Neurodegenerative Disease." Journal of Alzheimer's Disease 82, no. 4 (August 17, 2021): 1373–401. http://dx.doi.org/10.3233/jad-210198.

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Progressive neurodegenerative diseases represent some of the largest growing treatment challenges for public health in modern society. These diseases mainly progress due to aging and are driven by microglial surveillance and activation in response to changes occurring in the aging brain. The lack of efficacious treatment options for Alzheimer’s disease (AD), as the focus of this review, and other neurodegenerative disorders has encouraged new approaches to address neuroinflammation for potential treatments. Here we will focus on the increasing evidence that dysbiosis of the gut microbiome is characterized by inflammation that may carry over to the central nervous system and into the brain. Neuroinflammation is the common thread associated with neurodegenerative diseases, but it is yet unknown at what point and how innate immune function turns pathogenic for an individual. This review will address extensive efforts to identify constituents of the gut microbiome and their neuroactive metabolites as a peripheral path to treatment. This approach is still in its infancy in substantive clinical trials and requires thorough human studies to elucidate the metabolic microbiome profile to design appropriate treatment strategies for early stages of neurodegenerative disease. We view that in order to address neurodegenerative mechanisms of the gut, microbiome and metabolite profiles must be determined to pre-screen AD subjects prior to the design of specific, chronic titrations of gut microbiota with low-dose antibiotics. This represents an exciting treatment strategy designed to balance inflammatory microglial involvement in disease progression with an individual’s manifestation of AD as influenced by a coercive inflammatory gut.
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Marizzoni, Moira, Annamaria Cattaneo, Peppino Mirabelli, Cristina Festari, Nicola Lopizzo, Valentina Nicolosi, Elisa Mombelli, et al. "Short-Chain Fatty Acids and Lipopolysaccharide as Mediators Between Gut Dysbiosis and Amyloid Pathology in Alzheimer’s Disease." Journal of Alzheimer's Disease 78, no. 2 (November 10, 2020): 683–97. http://dx.doi.org/10.3233/jad-200306.

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Background: Metagenomic data support an association between certain bacterial strains and Alzheimer’s disease (AD), but their functional dynamics remain elusive. Objective: To investigate the association between amyloid pathology, bacterial products such as lipopolysaccharide (LPS) and short chain fatty acids (SCFAs: acetate, valerate, butyrate), inflammatory mediators, and markers of endothelial dysfunction in AD. Methods: Eighty-nine older persons with cognitive performance from normal to dementia underwent florbetapir amyloid PET and blood collection. Brain amyloidosis was measured with standardized uptake value ratio versus cerebellum. Blood levels of LPS were measured by ELISA, SCFAs by mass spectrometry, cytokines by using real-time PCR, and biomarkers of endothelial dysfunction by flow cytometry. We investigated the association between the variables listed above with Spearman’s rank test. Results: Amyloid SUVR uptake was positively associated with blood LPS (rho≥0.32, p≤0.006), acetate and valerate (rho≥0.45, p < 0.001), pro-inflammatory cytokines (rho≥0.25, p≤0.012), and biomarkers of endothelial dysfunction (rho≥0.25, p≤0.042). In contrast, it was negatively correlated with butyrate (rho≤–0.42, p≤0.020) and the anti-inflammatory cytokine IL10 (rho≤–0.26, p≤0.009). Endothelial dysfunction was positively associated with pro-inflammatory cytokines, acetate and valerate (rho≥0.25, p≤0.045) and negatively with butyrate and IL10 levels (rho≤–0.25, p≤0.038). Conclusion: We report a novel association between gut microbiota-related products and systemic inflammation with brain amyloidosis via endothelial dysfunction, suggesting that SCFAs and LPS represent candidate pathophysiologic links between the gut microbiota and AD pathology.
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Schmidt, Emma K. A., Pamela J. F. Raposo, Karen L. Madsen, Keith K. Fenrich, Gillian Kabarchuk, and Karim Fouad. "What Makes a Successful Donor? Fecal Transplant from Anxious-Like Rats Does Not Prevent Spinal Cord Injury-Induced Dysbiosis." Biology 10, no. 4 (March 24, 2021): 254. http://dx.doi.org/10.3390/biology10040254.

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Spinal cord injury (SCI) causes gut dysbiosis and an increased prevalence of depression and anxiety. Previous research showed a link between these two consequences of SCI by using a fecal transplant from healthy rats which prevented both SCI-induced microbiota changes and the subsequent development of anxiety-like behaviour. However, whether the physical and mental state of the donor are important factors in the efficacy of FMT therapy after SCI remains unknown. In the present study, rats received a fecal transplant following SCI from uninjured donors with increased baseline levels of anxiety-like behaviour and reduced proportion of Lactobacillus in their stool. This fecal transplant increased intestinal permeability, induced anxiety-like behaviour, and resulted in minor but long-term alterations in the inflammatory state of the recipients compared to vehicle controls. There was no significant effect of the fecal transplant on motor recovery in rehabilitative training, suggesting that anxiety-like behaviour did not affect the motivation to participate in rehabilitative therapy. The results of this study emphasize the importance of considering both the microbiota composition and the mental state of the donor for fecal transplants following spinal cord injury.
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Oleskin, A. V. "INTERACTION OF THE SYMBIOTIC MICROBIOTA OF THE GASTRO-INTESTINAL TRACT WITH THE NERVOUS SYSTEM OF THE HOST ORGANISM." Physical and rehabilitation medicine, medical rehabilitation 1, no. 2 (June 15, 2019): 90–100. http://dx.doi.org/10.36425/2658-6843-19193.

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Symbiotic microorganisms inhabit a wide variety of niches in the human organism. Of paramount importance is the microbiota of the gastro-intestinal (GI) tract, especially of its distal part (the colon). Bidirectional signal exchange proceeds within the microbiota-host system, and diverse microbial metabolites modify the functions of the nervous system via metabolic, genetic, and neuroendocrine pathways. Increasing attention is currently given to the role of the GI microbiota in terms of the host's physical and mental health; therefore, it has been suggested to replace the widely used term gut-brain axis with the new term microbiota-gut-brain axis. The GI microbiota directly interacts with the enteric nervous system (ENS) that represents a partly autonomous subdivision of the nervous system. An important role is also played by the GI tract-innervating vagus nerve. In addition, the influence of the microbiota on the nervous system can be mediated by the immune system. The microbiota impact on the nervous system of the host results in significant alterations in the host's behavior, mood, and even taste. In the literature, there is evidence that neurological and psychological diseases are linked to microecological disorders (dysbioses) in the GI tract. In particular, dysbioses with manifest GI symptoms are often accompanied by serious brain problems.
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Hata, Tomokazu, Noriyuki Miyata, Shu Takakura, Kazufumi Yoshihara, Yasunari Asano, Tae Kimura-Todani, Makoto Yamashita, et al. "The Gut Microbiome Derived From Anorexia Nervosa Patients Impairs Weight Gain and Behavioral Performance in Female Mice." Endocrinology 160, no. 10 (August 26, 2019): 2441–52. http://dx.doi.org/10.1210/en.2019-00408.

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Abstract Anorexia nervosa (AN) results in gut dysbiosis, but whether the dysbiosis contributes to AN-specific pathologies such as poor weight gain and neuropsychiatric abnormalities remains unclear. To address this, germ-free mice were reconstituted with the microbiota of four patients with restricting-type AN (gAN mice) and four healthy control individuals (gHC mice). The effects of gut microbes on weight gain and behavioral characteristics were examined. Fecal microbial profiles in recipient gnotobiotic mice were clustered with those of the human donors. Compared with gHC mice, gAN mice showed a decrease in body weight gain, concomitant with reduced food intake. Food efficiency ratio (body weight gain/food intake) was also significantly lower in gAN mice than in gHC mice, suggesting that decreased appetite as well as the capacity to convert ingested food to unit of body substance may contribute to poor weight gain. Both anxiety-related behavior measured by open-field tests and compulsive behavior measured by a marble-burying test were increased only in gAN mice but not in gHC mice. Serotonin levels in the brain stem of gAN mice were lower than those in the brain stem of gHC mice. Moreover, the genus Bacteroides showed the highest correlation with the number of buried marbles among all genera identified. Administration of Bacteroides vulgatus reversed compulsive behavior but failed to exert any substantial effect on body weight. Collectively, these results indicate that AN-specific dysbiosis may contribute to both poor weight gain and mental disorders in patients with AN.
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Guo, Mingyan, Jun Peng, Xiaoyan Huang, Lingjun Xiao, Fenyan Huang, and Zhiyi Zuo. "Gut Microbiome Features of Chinese Patients Newly Diagnosed with Alzheimer’s Disease or Mild Cognitive Impairment." Journal of Alzheimer's Disease 80, no. 1 (March 9, 2021): 299–310. http://dx.doi.org/10.3233/jad-201040.

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Background: Patients with Alzheimer’s disease (AD) have gut microbiome alterations compared with healthy controls. However, previous studies often assess AD patients who have been on medications or other interventions for the disease. Also, simultaneous determination of gut microbiome in patients with mild cognitive impairment (MCI) or AD in a study is rare. Objective: To determine whether there was a gut microbiome alteration in patients newly diagnosed with AD or MCI and whether the degree of gut microbiome alteration was more severe in patients with AD than patients with MCI. Methods: Fecal samples of 18 patients with AD, 20 patients with MCI, and 18 age-matched healthy controls were collected in the morning for 16S ribosomal RNA sequencing. No patient had medications or interventions for AD or MCI before the samples were collected. Results: Although there was no difference in the microbial α-diversity among the three groups, patients with AD or MCI had increased β-diversity compared with healthy controls. Patients with AD had decreased Bacteroides, Lachnospira, and Ruminiclostridium_9 and increased Prevotella at the genus level compared with healthy controls. The changing direction of these genera in patients with MCI was the same as patients with AD. However, Lachnospira was the only genus whose abundance in patients with MCI was statistically significantly lower than healthy controls. Bacteroides, Lachnospira, and Ruminiclostridium_9 were positively associated with better cognitive functions whereas Prevotella was on the contrary when subjects of all three groups were considered. The negative correlation of Prevotella with cognitive functions remained among patients with MCI. Conclusion: Patients newly diagnosed with AD or MCI have gut dysbiosis that includes the decrease of potentially protective microbiome, such as Bacteroides, and the increase of microbiome that can promote inflammation, such as Prevotella. Our results support a novel idea that the degree of gut dysbiosis is worsened with the disease stage from MCI to AD.
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Arneth, Borros M. "Gut–brain axis biochemical signalling from the gastrointestinal tract to the central nervous system: gut dysbiosis and altered brain function." Postgraduate Medical Journal 94, no. 1114 (July 19, 2018): 446–52. http://dx.doi.org/10.1136/postgradmedj-2017-135424.

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BackgroundThe gut–brain axis facilitates a critical bidirectional link and communication between the brain and the gut. Recent studies have highlighted the significance of interactions in the gut–brain axis, with a particular focus on intestinal functions, the nervous system and the brain. Furthermore, researchers have examined the effects of the gut microbiome on mental health and psychiatric well-being.The present study reviewed published evidence to explore the concept of the gut–brain axis.AimsThis systematic review investigated the relationship between human brain function and the gut–brain axis.MethodsTo achieve these objectives, peer-reviewed articles on the gut–brain axis were identified in various electronic databases, including PubMed, MEDLINE, CIHAHL, Web of Science and PsycINFO.ResultsData obtained from previous studies showed that the gut–brain axis links various peripheral intestinal functions to brain centres through a broad range of processes and pathways, such as endocrine signalling and immune system activation. Researchers have found that the vagus nerve drives bidirectional communication between the various systems in the gut–brain axis. In humans, the signals are transmitted from the liminal environment to the central nervous system.ConclusionsThe communication that occurs in the gut–brain axis can alter brain function and trigger various psychiatric conditions, such as schizophrenia and depression. Thus, elucidation of the gut–brain axis is critical for the management of certain psychiatric and mental disorders.
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Gao, Fengjie, Ruijin Guo, Qingyan Ma, Yening Li, Wei Wang, Yajuan Fan, Yanmei Ju, et al. "Stressful events induce long-term gut microbiota dysbiosis and associated post-traumatic stress symptoms in healthcare workers fighting against COVID-19." Journal of Affective Disorders 303 (April 2022): 187–95. http://dx.doi.org/10.1016/j.jad.2022.02.024.

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Vicentini, F., L. Griffin, C. Keenan, J. Cavin, K. Nieves, S. A. Hirota, and K. A. Sharkey. "A37 ENTERIC MICROBIOTA CONTRIBUTE TO BEHAVIORAL ALTERATIONS OBSERVED IN MICE WITH COLITIS." Journal of the Canadian Association of Gastroenterology 3, Supplement_1 (February 2020): 44–45. http://dx.doi.org/10.1093/jcag/gwz047.036.

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Abstract Background The enteric microbiota has been recognized as an essential regulator of both gut and brain physiology, a complex interaction generally termed the microbiota-gut-brain axis. Disturbances to gastrointestinal physiology lead to alterations in the composition of the enteric microbiota, whereas dysbiosis can also contribute to pathophysiology. Inflammatory bowel diseases (IBD) are chronic, relapsing inflammatory conditions of the gastrointestinal tract, associated with microbial dysbiosis. Interestingly, IBD patients exhibit an increased incidence of mental illness (i.e. anxiety and depression), often termed “sickness behavior”, even during the remitting phase of their disease. Nevertheless, it is unclear if alterations in the enteric microbiota associated with IBD are responsible for the observed modification in brain function and behavior. Here, we hypothesized that sickness behavior is driven by alterations in microbial composition, which occur in the context of intestinal inflammation. Aims We sought to determine whether transfer of the microbiota from colitic mice, exhibiting sickness behaviour, into healthy counterparts would induce behavioral changes. Methods Male mice (C57Bl/6J; 8 weeks old) were used in all experiments. Colitis was induced by administration of 2.5% dextran sodium sulfate (DSS) in the drinking water for 5 days. Colonic inflammation was assessed by measuring fecal lipocalin-2 and the expression of pro-inflammatory mediators via qPCR. Cecal matter from donor mice (control or DSS treated) were collected for fecal microbiota transplant (FMT). FMT was performed via oral gavage in antibiotic-treated recipient mice. Gut bacteria were evaluated by 16S rRNA sequencing in cecal samples. Anxiety- and depression-like behavior were assessed by elevated plus maze and tail suspension test, respectively. Results DSS-treated mice exhibited clinical disease, reflected by body weight loss, increased fecal lipocalin-2 and elevated colonic pro-inflammatory cytokine transcripts. An increase in anxiety-like behavior was observed in mice with colitis, although no alterations in depression-like behavior were detected. Colitic mice exhibited a unique microbial community. Transferring cecal material from colitic mice into recipient, antibiotic-treated mice, recapitulated alterations in behavior seen in colitic donors, as shown by increased anxiety-like behavior and unexpectedly, increased depression-like behavior. These behavioral changes occurred in the absence of colonic or brain inflammation in the recipient mice, but were associated with changes in stress-related gene expression (i.e. Crh). Conclusions Colitis-associated sickness behavior can be transmitted to antibiotic-treated recipient mice via FMT, which occurs in the absence of overt intestinal or brain inflammation. Funding Agencies CIHRNational Council for Scientific and Technological Development (CNPq-Brazil)
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Hu, Li, Shaoping Zhu, Xiaoping Peng, Kanglan Li, Wanjuan Peng, Yu Zhong, Chenyao Kang, Xingxing Cao, Zhou Liu, and Bin Zhao. "High Salt Elicits Brain Inflammation and Cognitive Dysfunction, Accompanied by Alternations in the Gut Microbiota and Decreased SCFA Production." Journal of Alzheimer's Disease 77, no. 2 (September 15, 2020): 629–40. http://dx.doi.org/10.3233/jad-200035.

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Background: Excessive salt intake is considered as an important risk factor for cognitive impairment, which might be the consequence of imbalanced intestinal homeostasis. Objective: To investigate the effects of dietary salt on the gut microbiota and cognitive performance and the underlying mechanisms. Methods: Adult female C57BL/6 mice were maintained on either normal chow (control group, CON) or sodium-rich chow containing 8% NaCl (high-salt diet, HSD) for 8 weeks. Spatial learning and memory ability, short-chain fatty acids (SCFAs) concentrations, gut bacterial flora composition, blood-brain barrier permeability, and proinflammatory cytokine levels and apoptosis in the brain were evaluated. Results: The mice fed a HSD for 8 weeks displayed impaired learning and memory abilities. HSD significantly reduced the proportions of Bacteroidetes (S24-7 and Alloprevotella) and Proteobacteria and increased that of Firmicutes (Lachnospiraceae and Ruminococcaceae). SCFA concentrations decreased in the absolute concentrations of acetate, propionate, and butyrate in the fecal samples from the HSD-fed mice. The HSD induced both BBB dysfunction and microglial activation in the mouse brain, and increased the IL-1β, IL-6, and TNF-α expression levels in the cortex. More importantly, the degree of apoptosis was higher in the cortex and hippocampus region of mice fed the HSD, and this effect was accompanied by significantly higher expression of cleaved caspase-3, caspase-3, and caspase-1. Conclusion: The HSD directly causes cognitive dysfunction in mice by eliciting an inflammatory environment and triggering apoptosis in the brain, and these effects are accompanied by gut dysbiosis, particularly reduced SCFA production.
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Kvasnová, S., D. Schierová, J. Mrázek, K. Olša Fliegerová, H. Tejkalová, and P. Kačer. "P.503 The influence of early dysbiosis on gut microbiome and brain neuroactive molecules." European Neuropsychopharmacology 29 (December 2019): S354. http://dx.doi.org/10.1016/j.euroneuro.2019.09.509.

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Lim, Mi Young, Seungpyo Hong, Jung-Ha Kim, and Young-Do Nam. "Association Between Gut Microbiome and Frailty in the Older Adult Population in Korea." Journals of Gerontology: Series A 76, no. 8 (January 13, 2021): 1362–68. http://dx.doi.org/10.1093/gerona/glaa319.

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Abstract Frailty is a common geriatric syndrome associated with the risk of adverse health outcomes. Recently, 2 key pathophysiological characteristics of frailty, altered energy metabolism and dysregulated immunity, have been reported to be associated with gut microbiome dysbiosis, indicating that the gut microbiome plays a role in frailty. However, few studies have directly examined the relationship between the gut microbiome and frailty. Here, we investigated the association of frailty measures with the gut microbiome using 16S rRNA gene sequencing data obtained from the fecal samples of 176 Korean older adults. Overall frailty was scored using the Korean Frailty Index (FI). Grip strength and Geriatric Depression Scale (GDS) scores were used as physical and mental frailty measures, respectively. In contrast to age, metabolic, and inflammatory biomarkers, the frailty measures were associated with interindividual variations in microbial composition (false discovery rate [FDR] &lt; 0.2). Both FI and GDS scores were negatively associated with microbial diversity (FDR &lt; 0.2). Frailty measures showed distinct associations with specific microbial taxa and metabolic functions. Particularly, the Bacteroides enterotype was found only in subjects categorized in the frail group. Moreover, we observed that the abundance of beneficial taxa, such as Prevotella copri and Coprococcus eutactus, was reduced in frailer individuals, whereas that of detrimental taxa, such as Bacteroides fragilis and Clostridium hathewayi, was increased (FDR &lt; 0.2). Our findings suggest that the gut microbiome can be used an indicator of an increased risk of frailty or a target for improving health in frail older adults.
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Cuervo-Zanatta, Daniel, Jaime Garcia-Mena, and Claudia Perez-Cruz. "Gut Microbiota Alterations and Cognitive Impairment Are Sexually Dissociated in a Transgenic Mice Model of Alzheimer’s Disease." Journal of Alzheimer's Disease 82, s1 (June 22, 2021): S195—S214. http://dx.doi.org/10.3233/jad-201367.

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Background: Normal aging is accompanied by cognitive deficiencies, affecting women and men equally. Aging is the main risk factor for Alzheimer’s disease (AD), with women having a higher risk. The higher prevalence of AD in women is associated with the abrupt hormonal decline seen after menopause. However, other factors may be involved in this sex-related cognitive decline. Alterations in gut microbiota (GM) and its bioproducts have been reported in AD subjects and transgenic (Tg) mice, having a direct impact on brain amyloid-β pathology in male (M), but not in female (F) mice. Objective: The aim of this work was to determine GM composition and cognitive dysfunction in M and F wildtype (WT) and Tg mice, in a sex/genotype segregation design. Methods: Anxiety, short term working-memory, spatial learning, and long-term spatial memory were evaluated in 6-month-old WT and Tg male mice. Fecal short chain fatty acids were determined by chromatography, and DNA sequencing and bioinformatic analyses were used to determine GM differences. Results: We observed sex-dependent differences in cognitive skills in WT mice, favoring F mice. However, the cognitive advantage of females was lost in Tg mice. GM composition showed few sex-related differences in WT mice. Contrary, Tg-M mice presented a more severe dysbiosis than Tg-F mice. A decreased abundance of Ruminococcaceae was associated with cognitive deficits in Tg-F mice, while butyrate levels were positively associated with better working- and object recognition-memory in WT-F mice. Conclusion: This report describes a sex-dependent association between GM alterations and cognitive impairment in a mice model of AD.
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Margret, Arockiya Anita, Madasamy Sukanya, Christinal Johnson, Subbiah Kulandaivel, and Natarajan Arun Nagendran. "Facilitating the gut brain axis by probiotic bacteria to modulate neuroimmune response on lead exposed zebra fish models." Acta Scientiarum. Health Sciences 43 (February 11, 2021): e52932. http://dx.doi.org/10.4025/actascihealthsci.v43i1.52932.

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Unravelling the efficacy of gut biome has a major impact on health. An unbalanced microbiome composition is linked to many common illnesses such as gut dysbiosis, mental deformities and immunological imbalance. An optimistic influence on the gut biome can be made by consuming probiotics. This would stimulate neuroprotection and immunomodulation intended by heavy metals pollution. Lead is a major source of neurotoxin that can induce neural deformities. Lactobacillus species isolated from curd were characterized to confirm its specificity. Zebra fish was reared at standard conditions and preclinical assessment on the intensity of induced neurotoxin lead was performed. The embryo toxic assay, immunomodulation effects and animal behavioural models endorsed the consequence of neurotoxicity. Different concentrations of bacterial isolate with standard antidepressant was considered for analysing the vigour of toxicity and its influence on cognitive behaviour by novel tank diving method. The restrain in the animal behaviour was also conferred by all the test samples with a decreased bottom dwelling time which was authenticated with haematology and histopathological studies. The alterations in morphology of the lymphocytes were balanced by the treated test samples. This study paves a twofold potential of probiotic as neuroprotectant and immune modulator against heavy metal toxicity.
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Ryu, Ji Yeon, Hyung Muk Choi, Hyung-In Yang, and Kyoung Soo Kim. "Dysregulated Autophagy Mediates Sarcopenic Obesity and Its Complications via AMPK and PGC1α Signaling Pathways: Potential Involvement of Gut Dysbiosis as a Pathological Link." International Journal of Molecular Sciences 21, no. 18 (September 19, 2020): 6887. http://dx.doi.org/10.3390/ijms21186887.

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Sarcopenic obesity (SOB), which is closely related to being elderly as a feature of aging, is recently gaining attention because it is associated with many other age-related diseases that present as altered intercellular communication, dysregulated nutrient sensing, and mitochondrial dysfunction. Along with insulin resistance and inflammation as the core pathogenesis of SOB, autophagy has recently gained attention as a significant mechanism of muscle aging in SOB. Known as important cellular metabolic regulators, the AMP-activated protein kinase (AMPK) and the peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1α) signaling pathways play an important role in autophagy, inflammation, and insulin resistance, as well as mutual communication between skeletal muscle, adipose tissue, and the liver. Furthermore, AMPK and PGC-1α signaling pathways are implicated in the gut microbiome–muscle axis. In this review, we describe the pathological link between SOB and its associated complications such as metabolic, cardiovascular, and liver disease, falls and fractures, osteoarthritis, pulmonary disease, and mental health via dysregulated autophagy controlled by AMPK and/or PGC-1α signaling pathways. Here, we propose potential treatments for SOB by modulating autophagy activity and gut dysbiosis based on plausible pathological links.
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Fetarayani, Deasy, Handoko Hariyono, and Gatot Soegiarto. "The role of gut microbiota in health and diseases." Qanun Medika - Medical Journal Faculty of Medicine Muhammadiyah Surabaya 5, no. 1 (January 26, 2021): 19. http://dx.doi.org/10.30651/jqm.v5i1.5846.

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ABSTRACTABSTRACTMicrobiota contributes a crucial part in the human hosts' health and actively provides to the emergence of various diseases. The optimal composition of healthy intestinal microbiota varies from person to person. The more various and abundant of the microbiota, the greater their resistance to outside hazards. Colonization of the microbiota in the human body starts after delivery and develops continuously from infant to adult. The largest microbial colony is constructed in the lower part of the adult human digestive tract. The composition of the human intestinal microbiota alters promptly during the beginning of life and is steady. It has been described the close relationship among dysbiosis of the intestinal microbiota with intestinal and non-intestinal diseases. Nevertheless, it is uncertain whether dysbiosis is the culprit of the disease or only as a result of the disease. Human microbiota's role must be investigated more deeply so that later it can be developed for the prevention, diagnosis of disease, and more effective treatment strategies in the future. In this minireview, we will describe the development of the gut microbiota, its interaction with our bodily systems and defense, the multiple causes of dysbiosis, and its impact on several metabolic in inflammatory diseases in humans. With this insight, it is hoped that we can be more cautious about using antibiotics, avoid things that lead to dysbiosis, and handle diseases more holistically, putting the balance of the microbiota into account. Keywords: human, microbiota, gastrointestinal tract, dysbiosis, health and diseaseCorresponding author: deasyfetarayani@gmail.com
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Harris, Cailin, Peter T. Kim, Dawn Waterhouse, Zeny Feng, Jessmyn Niergarth, and Christine H. Lee. "Precision medicine and gut dysbiosis." Healthcare Management Forum 33, no. 3 (January 14, 2020): 107–10. http://dx.doi.org/10.1177/0840470419899426.

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Clostridioides difficile Infection (CDI) is a leading cause of healthcare-associated infections in Canada, affecting the gastrointestinal tract which can lead to fever, abdominal pain, and diarrhea. Effective treatment for patients with Recurrent CDI (rCDI) can be achieved by Fecal Microbiota Transplantation (FMT) by introducing the gut micro-organisms of a healthy person (donor) into the bowel of the affected individual. Research has shown that an increase in the specific bacterial phyla post-FMT may be partly responsible for this gut restoration and elimination of disease. Furthermore, in understanding the key bacteria associated with successful FMT, full treatment plans can be developed for the individual needs of the patient by matching an infected individual with a donor possessing ideal microbiota for the specific patient. This development of precision medicine and more systematic adoption of FMT can be the next step toward more rapid resolution of rCDI.
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Choudhary, Arbind Kumar, and Yeong Lee. "Dysregulated microbiota-gut-brain axis." Nutrition & Food Science 47, no. 5 (September 11, 2017): 648–58. http://dx.doi.org/10.1108/nfs-03-2017-0034.

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Purpose This paper aims to summarize the available literatures, specifically in the following areas: metabolic and other side effects of aspartame; microbiota changes/dysbiosis and its effect on the gut-brain axis; changes on gut microbiota as a result of aspartame usage; metabolic effects (weight gain and glucose intolerance) of aspartame due to gut dysbiosis; and postulated effects of dysregulated microbiota-gut-brain axis on other aspartame side-effects (neurophysiological symptoms and immune dysfunction). Design/methodology/approach Aspartame is rapidly becoming a public health concern because of its purported side-effects especially neurophysiological symptom and immune dysregulation. It is also paradoxical that metabolic consequences including weight gain and impaired blood glucose levels have been observed in consumers. Exact mechanisms of above side-effects are unclear, and data are scarce but aspartame, and its metabolites may have caused disturbance in the microbiota-gut-brain axis. Findings Additional studies investigating the impact of aspartame on gut microbiota and metabolic health are needed. Originality/value Exact mechanism by which aspartame-induced gut dysbiosis and metabolic dysfunction requires further investigation.
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Kadim, Muzal, and Bertri Maulidya Masita. "The importance of gut health in early life for long term health." World Nutrition Journal 5, S2 (January 31, 2022): 1–8. http://dx.doi.org/10.25220/wnj.v05.s2.0001.

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Introduction. The gut microbiota plays an important role in the normal functioning of the host organism. The microbiota of healthy newborn affected by many factors such as prenatal exposures, maternal nutrition, mode of delivery, type of feeding, introduction to solid food and its type, geography, and antibiotics consumption; and its composition continues to mature until reaching 3 years of age. Normal gut microbiota is essential in gut health, and play an important role in our homeostasis. Therefore, gut microbiota is considered a crucial factor for proper early life development and lifelong health. Prebiotics, along with probiotics, may alter gut microbiota composition thus play a role in the prevention of various diseases associated with dysbiosis condition. Methods. Advanced search for relevant literatures in PubMed, Cochrane, and Willey was conducted. After assessing the relevancy and eligibility, articles were selected and critically appraised. Conclusions. Accumulating evidence from different studies has shown that the occurrence of a disease is often preceded by early alterations of the microbiota. Many studies established correlation between gut microbiota dysbiosis with diseases pathogenesis i.e obesity and other metabolic syndrome, asthma and allergies, also stress-related disorder. Prebiotic supplementation has proven to be effective in obesity, asthma and allergies management, also beneficial for immune system.
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Seo, Ye Seul, Hye-Bin Lee, Yoonsook Kim, and Ho-Young Park. "Dietary Carbohydrate Constituents Related to Gut Dysbiosis and Health." Microorganisms 8, no. 3 (March 18, 2020): 427. http://dx.doi.org/10.3390/microorganisms8030427.

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Recent studies report that microbiota in the human intestine play an important role in host health and that both long- and short-term diets influence gut microbiota. These findings have fueled interest in the potential of food to promote health by shaping the intestinal microbiota. Despite the fact that large populations in Asia consume high quantities of carbohydrates, such diets have been ignored in comparison to the attention received by Western diets containing high quantities of fat and animal protein. We gathered data that suggest an association between imbalanced high-carbohydrate intake and gut microbiota and host health. In this review, we identify not only the effect of total carbohydrates on the intestinal microbiota specifically and the health of their hosts in general, but also how specific types of carbohydrates influence both factors.
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Mendez-Figueroa, Vanessa, Jose Biscaia, Rosa Mohedano, Ascension Blanco-Fernandez, Maria Bailen, Carlo Bressa, Mar Larrosa, and Rocio Gonzalez-Soltero. "Can Gut Microbiota and Lifestyle Help Us in the Handling of Anorexia Nervosa Patients?" Microorganisms 7, no. 2 (February 22, 2019): 58. http://dx.doi.org/10.3390/microorganisms7020058.

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Gut microbiota is composed of different microorganisms that play an important role in the host. New research shows that bidirectional communications happen between intestinal microbiota and the brain, which is known as the gut–brain axis. This communication is significant and could have a negative or positive effect depending on the state of the gut microbiota. Anorexia nervosa (AN) is a mental illness associated with metabolic, immunologic, biochemical, sensory abnormalities, and extremely low body weight. Different studies have shown a dysbiosis in patients with AN. Due to the gut–brain axis, it was observed that some of the symptoms could be improved in these patients by boosting their gut microbiota. This paper highlights some evidence connecting the role of microbiota in the AN onset and disease progress. Finally, a proposal is done to include the microbiota analysis as part of the recovery protocol used to treat AN patients. When conducting clinical studies of gut microbiota in AN patients, dysbiosis is expected to be found. Then the prescription of a personalized treatment rich in prebiotics and probiotics could be proposed to reverse the dysbiosis.
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Lyu, Yi, Lei Wu, Fang Wang, Xinchun Shen, and Dingbo Lin. "Carotenoid supplementation and retinoic acid in immunoglobulin A regulation of the gut microbiota dysbiosis." Experimental Biology and Medicine 243, no. 7 (March 13, 2018): 613–20. http://dx.doi.org/10.1177/1535370218763760.

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Dysbiosis, a broad spectrum of imbalance of the gut microbiota, may progress to microbiota dysfunction. Dysbiosis is linked to some human diseases, such as inflammation-related disorders and metabolic syndromes. However, the underlying mechanisms of the pathogenesis of dysbiosis remain elusive. Recent findings suggest that the microbiome and gut immune responses, like immunoglobulin A production, play critical roles in the gut homeostasis and function, and the progression of dysbiosis. In the past two decades, much progress has been made in better understanding of production of immunoglobulin A and its association with commensal microbiota. The present minireview summarizes the recent findings in the gut microbiota dysbiosis and dysfunction of immunoglobulin A induced by the imbalance of pathogenic bacteria and commensal microbiota. We also propose the potentials of dietary carotenoids, such as β-carotene and astaxanthin, in the improvement of the gut immune system maturation and immunoglobulin A production, and the consequent promotion of the gut health. Impact statement The concept of carotenoid metabolism in the gut health has not been well established in the literature. Here, we review and discuss the roles of retinoic acid and carotenoids, including pro-vitamin A carotenoids and xanthophylls in the maturation of the gut immune system and IgA production. This is the first review article about the carotenoid supplements and the metabolites in the regulation of the gut microbiome. We hope this review would provide a new direction for the management of the gut microbiota dysbiosis by application of bioactive carotenoids and the metabolites.
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Yamashiro, Yuichiro. "Gut Microbiota in Health and Disease." Annals of Nutrition and Metabolism 71, no. 3-4 (2017): 242–46. http://dx.doi.org/10.1159/000481627.

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Intestinal regulatory T (Treg) cells are critical to maintaining immune tolerance to dietary antigens and gut microbiota. This paper reviews several papers on this topic that were recently published by Japanese researchers. Specifically, Prof. K. Honda and his group have found that commensal microbiota capable of metabolizing butyrate induces the differentiation of colonic Treg cells. In a separate work, Prof. Y. Yokoyama and his group used a novel, culture-independent analytical method (the Yakult Intestinal Flora-Scan) for detection of bacteria in the bloodstream. Their work revealed that bacteremia in invasive surgery patients was ameliorated by synbiotic supplementation; similar results were reported in pediatric surgical cases by Dr. T. Okazaki and his group. This cutting-edge method may lead to the evolution of an altered disease concept; an example of this change is provided by the description of bacteremia in patients with type 2 diabetes, as reported by Dr. J. Sato and her group. In a similar work, Prof. Y. Yamashiro and his group found that infants born by cesarean (C)-section, who typically have gut dysbiosis, exhibit higher carriage of toxigenic Clostridium perfringens. The finding suggests that C-section-born infants may serve as a potential reservoir of this opportunistic pathogen. Another separate work by the laboratory of Dr. K. Yamashiro has revealed that gut dysbiosis is associated with altered metabolism and systemic inflammation in patients with ischemic stroke. These papers are consistent with a study by Prof. N. Sudo and his group, who have made significant progress in research on interaction among the microbiota, gut, and brain.
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Sędzikowska, Aleksandra, and Leszek Szablewski. "Human Gut Microbiota in Health and Selected Cancers." International Journal of Molecular Sciences 22, no. 24 (December 14, 2021): 13440. http://dx.doi.org/10.3390/ijms222413440.

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The majority of the epithelial surfaces of our body, and the digestive tract, respiratory and urogenital systems, are colonized by a vast number of bacteria, archaea, fungi, protozoans, and viruses. These microbiota, particularly those of the intestines, play an important, beneficial role in digestion, metabolism, and the synthesis of vitamins. Their metabolites stimulate cytokine production by the human host, which are used against potential pathogens. The composition of the microbiota is influenced by several internal and external factors, including diet, age, disease, and lifestyle. Such changes, called dysbiosis, may be involved in the development of various conditions, such as metabolic diseases, including metabolic syndrome, type 2 diabetes mellitus, Hashimoto’s thyroidis and Graves’ disease; they can also play a role in nervous system disturbances, such as multiple sclerosis, Alzheimer’s disease, Parkinson’s disease, and depression. An association has also been found between gut microbiota dysbiosis and cancer. Our health is closely associated with the state of our microbiota, and their homeostasis. The aim of this review is to describe the associations between human gut microbiota and cancer, and examine the potential role of gut microbiota in anticancer therapy.
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