Journal articles: 'Leaky-gut syndrome'

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Obrenovich, Mark. "Leaky Gut, Leaky Brain?" Microorganisms 6, no. 4 (October 18, 2018): 107. http://dx.doi.org/10.3390/microorganisms6040107.

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‘Leaky gut’ syndrome, long-associated with celiac disease, has attracted much attention in recent years and for decades, was widely known in complementary/alternative medicine circles. It is often described as an increase in the permeability of the intestinal mucosa, which could allow bacteria, toxic digestive metabolites, bacterial toxins, and small molecules to ‘leak’ into the bloodstream. Nervous system involvement with celiac disease is know to occur even at subclinical levels. Gluten and gluten sensitivity are considered to trigger this syndrome in individuals genetically predisposed to celiac disease. However, the incidence of celiac disease in the general population is quite low. Nevertheless, increased public interest in gluten sensitivity has contributed to expanded food labels stating ‘gluten-free’ and the proliferation of gluten-free products, which further drives gluten-free lifestyle changes by individuals without frank celiac disease. Moreover, systemic inflammation is associated with celiac disease, depression, and psychiatric comorbidities. This mini-review focuses on the possible neurophysiological basis of leaky gut; leaky brain disease; and the microbiota’s contribution to inflammation, gastrointestinal, and blood-brain barrier integrity, in order to build a case for possible mechanisms that could foster further ‘leaky’ syndromes. We ask whether a gluten-free diet is important for anyone or only those with celiac disease.

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Kim, Kyu-Nam, and Kwang-Min Kim. "Leaky Gut Syndrome." Korean Journal of Family Practice 10, no. 5 (October 20, 2020): 316–23. http://dx.doi.org/10.21215/kjfp.2020.10.5.316.

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Park, Junghyun, Tae Joon Choi, Ki Sung Kang, and Seo-Hyung Choi. "The Interrelationships between Intestinal Permeability and Phlegm Syndrome and Therapeutic Potential of Some Medicinal Herbs." Biomolecules 11, no. 2 (February 15, 2021): 284. http://dx.doi.org/10.3390/biom11020284.

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The gastrointestinal (GI) tract has an intriguing and critical role beyond digestion in both modern and complementary and alternative medicine (CAM), as demonstrated by its link with the immune system. In this review, we attempted to explore the interrelationships between increased GI permeability and phlegm, an important pathological factor in CAM, syndrome, and therapeutic herbs for two disorders. The leaky gut and phlegm syndromes look considerably similar with respect to related symptoms, diseases, and suitable herbal treatment agents, including phytochemicals even though limitations to compare exist. Phlegm may be spread throughout the body along with other pathogens via the disruption of the GI barrier to cause several diseases sharing some parts of symptoms, diseases, and mechanisms with leaky gut syndrome. Both syndromes are related to inflammation and gut microbiota compositions. Well-designed future research should be conducted to verify the interrelationships for evidence based integrative medicine to contribute to the promotion of public health. In addition, systems biology approaches should be adopted to explore the complex synergistic effects of herbal medicine and phytochemicals on conditions associated with phlegm and leaky gut syndromes.

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Brom, B. "Integrative medicine and leaky gut syndrome." South African Family Practice 52, no. 4 (July 2010): 314–16. http://dx.doi.org/10.1080/20786204.2010.10873997.

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Farshchi, Masoumeh Kaboli, Farahzad Jabbari Azad, Roshanak Salari, Majid Mirsadraee, and Majid Anushiravani. "A Viewpoint on the Leaky Gut Syndrome to Treat Allergic Asthma: A Novel Opinion." Journal of Evidence-Based Complementary & Alternative Medicine 22, no. 3 (December 22, 2016): 378–80. http://dx.doi.org/10.1177/2156587216682169.

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Asthma is a common respiratory disease characterized by airway inflammation, airway hyperreactivity, and reversible airflow obstruction. Despite current treatments, the prevalence of asthma has increased markedly over decades. According to the theories proposed to explain the pathophysiology of autoimmune diseases in integrative medicine, leaky gut syndrome is a phenomenon of increased intestinal permeability due to the disruption of tight junctions and is thought to be related to many chronic diseases, such as food intolerance, inflammatory bowel disease, rheumatoid arthritis, asthma, and other autoimmune disease. One of the classical approaches used by integrative physicians to treat leaky gut syndrome is to repair intestinal permeability to prevent allergic cascade. Due to several mechanisms that have been mentioned in the protective effects of plant gums and plantain family seeds on the intestinal epithelium, we can propose an effective management for leaky gut syndrome to treat asthma.

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Rodina, Jekaterina, and Aleksejs Derovs. "Establishing the cut-offs of leaky gut syndrome diagnostic: where are we now?" Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences. 76, no. 5-6 (December 1, 2022): 569–77. http://dx.doi.org/10.2478/prolas-2022-0089.

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Abstract Gastrointestinal mucosa forms a surface that interacts with many external factors. Beside the digestion and absorption of nutrients, it also acts as a barrier to allergens, pathogens, and toxins. Leaky gut syndrome is defined as a gut mucosal barrier dysfunction, which results in abnormally increased intestinal permeability. Research shows that leaky gut syndrome (LGS) has a pathogenetic relationship with a series of gastrointestinal and extra-intestinal disorders. This review discusses the current understanding of intestinal barrier composition and pathological contribution of LGS to various diseases. The major aim of this paper is to review different methods for diagnostics and evaluation of intestinal wall permeability, identifying their priorities and disadvantages.

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Chernyavskyi, V. V., L. L. Pavlovskyi, and V. V. Tishchenko. "Leaky gut syndrome in the general clinical practice." Modern Gastroenterology, no. 3 (May 19, 2020): 91–95. http://dx.doi.org/10.30978/mg-2020-3-91.

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Twardowska, Agata, Adam Makaro, Agata Binienda, Jakub Fichna, and Maciej Salaga. "Preventing Bacterial Translocation in Patients with Leaky Gut Syndrome: Nutrition and Pharmacological Treatment Options." International Journal of Molecular Sciences 23, no. 6 (March 16, 2022): 3204. http://dx.doi.org/10.3390/ijms23063204.

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Leaky gut syndrome is a medical condition characterized by intestinal hyperpermeability. Since the intestinal barrier is one of the essential components maintaining homeostasis along the gastrointestinal tract, loss of its integrity due to changes in bacterial composition, decreased expression levels of tight junction proteins, and increased concentration of pro-inflammatory cytokines may lead to intestinal hyperpermeability followed by the development of gastrointestinal and non-gastrointestinal diseases. Translocation of microorganisms and their toxic metabolites beyond the gastrointestinal tract is one of the fallouts of the leaky gut syndrome. The presence of intestinal bacteria in sterile tissues and distant organs may cause damage due to chronic inflammation and progression of disorders, including inflammatory bowel diseases, liver cirrhosis, and acute pancreatitis. Currently, there are no medical guidelines for the treatment or prevention of bacterial translocation in patients with the leaky gut syndrome; however, several studies suggest that dietary intervention can improve barrier function and restrict bacteria invasion. This review contains current literature data concerning the influence of diet, dietary supplements, probiotics, and drugs on intestinal permeability and bacterial translocation.

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Simeonova, Denitsa, Mariya Ivanovska, Mariana Murdjeva, Andre F. Carvalho, and Michael Maes. "Recognizing the Leaky Gut as a Trans-diagnostic Target for Neuroimmune Disorders Using Clinical Chemistry and Molecular Immunology Assays." Current Topics in Medicinal Chemistry 18, no. 19 (December 21, 2018): 1641–55. http://dx.doi.org/10.2174/1568026618666181115100610.

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Background: Increased intestinal permeability with heightened translocation of Gramnegative bacteria, also known as “leaky gut”, is associated with the pathophysiology of neuroimmune disorders, such as Major Depressive Disorder (MDD), Chronic Fatigue Syndrome (CSF) and (deficit) schizophrenia, as well as with general medical disorders, including irritable bowel syndrome. This review aims to summarize clinical biochemistry and molecular immunology tests that may aid in the recognition of leaky gut in clinical practice. <p> Methods: We searched online libraries, including PubMed/MEDLINE, Google Scholar and Scopus, with the key words “diagnosis” or “biomarkers” and “leaky gut”, “bacterial translocation”, and “intestinal permeability” and focused on papers describing tests that may aid in the clinical recognition of leaky gut. <p> Results: To evaluate tight junction barrier integrity, serum IgG/IgA/IgM responses to occludin and zonulin and IgA responses to actomyosin should be evaluated. The presence of cytotoxic bacterial products in serum can be evaluated using IgA/IgM responses to sonicated samples of common Gram-negative gut commensal bacteria and assays of serum lipopolysaccharides (LPSs) and other bacterial toxins, including cytolethal distenting toxin, subunit B. Major factors associated with increased gut permeability, including gut dysbiosis and yeast overgrowth, use of NSAIDs and alcohol, food hypersensitivities (IgE-mediated), food intolerances (IgG-mediated), small bacterial overgrowth (SIBO), systemic inflammation, psychosocial stressors, some infections (e.g., HIV) and dietary patterns, should be assessed. Stool samples can be used to assay gut dysbiosis, gut inflammation and decreased mucosal defenses using assays of fecal growth of bacteria, yeast and fungi and stool assays of calprotectin, secretory IgA, β-defensin, α- antitrypsin, lysozyme and lactoferrin. Blood and breath tests should be used to exclude common causes of increased gut permeability, namely, food hypersensitivities and intolerances, SIBO, lactose intolerance and fructose malabsorption. <p> Discussion: Here, we propose strategies to recognize “leaky gut” in a clinical setting using the most adequate clinical chemistry and molecular immunology assays.

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Roorda, Andrew K., S. Gill Kanwar Rupinder, Terrie Mendelson, Daniel L. Peterson, Margaret Allen, and Kenneth F. Binmoeller. "Wireless Capsule Endoscopy in Patients with Leaky Gut Syndrome." Gastrointestinal Endoscopy 63, no. 5 (April 2006): AB172. http://dx.doi.org/10.1016/j.gie.2006.03.365.

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Lee, Jin-Cheoul, Sang-Kyun Park, and Jung-Kyun Bang. "Study on the Relationship between Dae-Jang-Jung-Gyeok(大腸正格) and Leaky Gut Syndrome." Journal of Korean Medical classics 26, no. 4 (November 25, 2013): 105–16. http://dx.doi.org/10.14369/skmc.2013.26.4.105.

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Park, Jong-Min, Young-Min Han, and Ki Baik Hahm. "PPI Aggravated Leaky Gut Syndrome, While P-CAB Did Not." Gastroenterology 152, no. 5 (April 2017): S505—S506. http://dx.doi.org/10.1016/s0016-5085(17)31869-3.

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Aleman, Ricardo Santos, Marvin Moncada, and Kayanush J. Aryana. "Leaky Gut and the Ingredients That Help Treat It: A Review." Molecules 28, no. 2 (January 7, 2023): 619. http://dx.doi.org/10.3390/molecules28020619.

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The human body is in daily contact with potentially toxic and infectious substances in the gastrointestinal tract (GIT). The GIT has the most significant load of antigens. The GIT can protect the intestinal integrity by allowing the passage of beneficial agents and blocking the path of harmful substances. Under normal conditions, a healthy intestinal barrier prevents toxic elements from entering the blood stream. However, factors such as stress, an unhealthy diet, excessive alcohol, antibiotics, and drug consumption can compromise the composition of the intestinal microbiota and the homeostasis of the intestinal barrier function of the intestine, leading to increased intestinal permeability. Intestinal hyperpermeability can allow the entry of harmful agents through the junctions of the intestinal epithelium, which pass into the bloodstream and affect various organs and systems. Thus, leaky gut syndrome and intestinal barrier dysfunction are associated with intestinal diseases, such as inflammatory bowel disease and irritable bowel syndrome, as well as extra-intestinal diseases, including heart diseases, obesity, type 1 diabetes mellitus, and celiac disease. Given the relationship between intestinal permeability and numerous conditions, it is convenient to seek an excellent strategy to avoid or reduce the increase in intestinal permeability. The impact of dietary nutrients on barrier function can be crucial for designing new strategies for patients with the pathogenesis of leaky gut-related diseases associated with epithelial barrier dysfunctions. In this review article, the role of functional ingredients is suggested as mediators of leaky gut-related disorders.

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Strahm, Anna M., and Lisa M. Christian. "Leaky gut syndrome, body mass and inflammation during pregnancy and postpartum." Brain, Behavior, and Immunity 98 (November 2021): 48. http://dx.doi.org/10.1016/j.bbi.2021.08.180.

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de Waal, Greta M. "The Link Between Bacterial Inflammagens, Leaky Gut Syndrome and Colorectal Cancer." Current Medicinal Chemistry 28, no. 41 (2021): 8534–48. http://dx.doi.org/10.2174/1875533xmte0pmzkw3.

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Park, Jong M., Ho J. Lee, Predrag Sikiric, and Ki B. Hahm. "BPC 157 Rescued NSAID-cytotoxicity Via Stabilizing Intestinal Permeability and Enhancing Cytoprotection." Current Pharmaceutical Design 26, no. 25 (August 4, 2020): 2971–81. http://dx.doi.org/10.2174/1381612826666200523180301.

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The stable gastric pentadecapeptide BPC 157 protects stomach cells, maintains gastric integrity against various noxious agents such as alcohol, nonsteroidal anti-inflammatory drugs (NSAIDs), and exerts cytoprotection/ adaptive cytoprotection/organoprotection in other epithelia, that is, skin, liver, pancreas, heart, and brain. Especially BPC 157 counteracts gastric endothelial injury that precedes and induces damage to the gastric epithelium and generalizes "gastric endothelial protection" to protection of the endothelium of other vessels including thrombosis, prolonged bleeding, and thrombocytopenia. In this background, we put the importance of BPC 157 as a possible way of securing GI safety against NSAIDs-induced gastroenteropathy since still unmet medical needs to mitigate NSAIDs-induced cytotoxicity are urgent. Furthermore, gastrointestinal irritants such as physical or mental stress, NSAIDs administration, surfactants destroyer such as bile acids, alcohol can lead to leaky gut syndrome through increasing epithelial permeability. In this review article, we described the potential rescuing actions of BPC 157 against leaky gut syndrome after NSAIDs administration for the first time.

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Ukrainets, R. V., and Yu S. Korneva. "Intestinal Microbiota, Leaky Gut Syndrome and New Interpretation of Pathogenesis and Prophylaxis of Well-Known Diseases (Review)." Medicina 8, no. 1 (2020): 20–33. http://dx.doi.org/10.29234/2308-9113-2020-8-1-20-33.

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Yang, Xiaochun, Shuyun Rao, Xiyan Xiang, Kazufumi Ohshiro, Krishanu Bhowmick, Bryan N. Nguyen, Keith A. Crandall, Patricia S. Latham, Kirti Shetty, and Lopa Mishra. "594: ALDH2-/-SPTBN1+/- MICE DEVELOP A PRO-INFLAMMATORY GUT MICROBIOME, LEAKY GUT, METABOLIC SYNDROME, AND NASH." Gastroenterology 162, no. 7 (May 2022): S—148—S—149. http://dx.doi.org/10.1016/s0016-5085(22)60356-1.

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Akiba, Yasutada, Koji Maruta, Takeshi Takajo, Kazuyuki Narimatsu, Hyder Said, Ikuo Kato, Atsukazu Kuwahara, and Jonathan D. Kaunitz. "Lipopolysaccharides transport during fat absorption in rodent small intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 318, no. 6 (June 1, 2020): G1070—G1087. http://dx.doi.org/10.1152/ajpgi.00079.2020.

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We report direct in vivo confirmation of transcellular lipopolysaccharides (LPS) uptake from the intestine into the portal vein (PV) involving CD36 and lipid rafts, with minor uptake via the canonical chylomicron pathway. The gut hormone glucagon-like peptide-2 (GLP-2) inhibited uptake into the PV. These data suggest that the bulk of LPS absorption is via the PV to the liver, helping clarify the mechanism of LPS transport into the PV as part of the “gut-liver” axis. These data do not support the paracellular transport of LPS, which has been implicated in the pathogenesis of the “leaky gut” syndrome.

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Mandarano, Alexandra H., Ludovic Giloteaux, Betsy A. Keller, Susan M. Levine, and Maureen R. Hanson. "Eukaryotes in the gut microbiota in myalgic encephalomyelitis/chronic fatigue syndrome." PeerJ 6 (January 22, 2018): e4282. http://dx.doi.org/10.7717/peerj.4282.

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Patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) often suffer from gastrointestinal symptoms and many are diagnosed with irritable bowel syndrome (IBS). Previous studies, including from our laboratory, have demonstrated that the ME/CFS gut bacterial composition is altered and less diverse when compared to healthy individuals. Patients have increased biomarkers of inflammation and leaky gut syndrome. To further investigate dysbiosis in the ME/CFS gut microbiome, we sought to characterize the eukaryotes present in the gut of 49 individuals with ME/CFS and 39 healthy controls. Using 18S rRNA sequencing, we have identified eukaryotes in stool samples of 17 healthy individuals and 17 ME/CFS patients. Our analysis demonstrates a small, nonsignificant decrease in eukaryotic diversity in ME/CFS patients compared to healthy individuals. In addition, ME/CFS patients show a nonsignificant increase in the ratio of fungal phyla Basidiomycota to Ascomycota, which is consistent with ongoing inflammation in ME/CFS. We did not identify specific eukaryotic taxa that are associated with ME/CFS disease status.

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Kostoglod, T. V., T. S. Krolevets, and M. A. Livzan. "A New Look at the Pathogenesis and Possibilities of Treatment and Prevention of Autoimmune Diseases with the Role of the Intestinal Barrier and Increased Intestinal Permeability." Effective Pharmacotherapy 17, no. 4 (April 18, 2021): 82–88. http://dx.doi.org/10.33978/2307-3586-2021-17-4-82-88.

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We described components of the intestinal barrier that maintains to integrity and assess their contribution and development of leaky gut syndrome. The relationship between intestinal permeability syndrome and excessive bacterial translocation with autoimmune diseases such as celiac disease, inflammatory bowel disease, type 1 diabetes mellitus, autoimmune hepatitis, and systemic lupus erythematosus were analyzed. The reasons for the occurrence of this syndrome were considered, its importance in the occurrence of these diseases, as well as in the development of therapeutic and preventive measures, was determined.

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Ozaka, Sotaro, Akira Sonoda, Shimpei Ariki, Mizuki Minata, Naganori Kamiyama, Shinya Hidano, Nozomi Sachi, et al. "Saireito, a Japanese herbal medicine, alleviates leaky gut associated with antibiotic-induced dysbiosis in mice." PLOS ONE 17, no. 6 (June 15, 2022): e0269698. http://dx.doi.org/10.1371/journal.pone.0269698.

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Antibiotics disrupt normal gut microbiota and cause dysbiosis, leading to a reduction in intestinal epithelial barrier function. Disruption of the intestinal epithelial barrier, which is known as “leaky gut”, results in increased intestinal permeability and contributes to the development or exacerbation of gastrointestinal diseases such as inflammatory bowel disease and irritable bowel syndrome. We have previously reported on a murine model of intestinal epithelial barrier dysfunction associated with dysbiosis induced by the administration of ampicillin and vancomycin. Saireito, a traditional Japanese herbal medicine, is often used to treat autoimmune disorders including ulcerative colitis; the possible mechanism of action and its efficacy, however, remains unclear. In this study, we examined the efficacy of Saireito in our animal model for leaky gut associated with dysbiosis. C57BL/6 mice were fed a Saireito diet for the entirety of the protocol (day1-28). To induce colitis, ampicillin and vancomycin were administered in drinking water for the last seven consecutive days (day22-28). As previously demonstrated, treatment with antibiotics caused fecal occult bleeding, cecum enlargement with black discoloration, colon inflammation with epithelial cell apoptosis, and upregulation of pro-inflammatory cytokines. Oral administration of Saireito significantly improved antibiotics-induced fecal occult bleeding and cecum enlargement by suppressing inflammation in the colon. Furthermore, Saireito treatment ensured the integrity of the intestinal epithelial barrier by suppressing apoptosis and inducing cell adhesion proteins including ZO-1, occludin, and E-cadherin in intestinal epithelial cells, which in turn decreased intestinal epithelial permeability. Moreover, the reduced microbial diversity seen in the gut of mice treated with antibiotics was remarkably improved with the administration of Saireito. In addition, Saireito altered the composition of gut microbiota in these mice. These results suggest that Saireito alleviates leaky gut caused by antibiotic-induced dysbiosis. Our findings provide a potentially new therapeutic strategy for antibiotic-related gastrointestinal disorders.

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Mason, Charles J., Swayamjit Ray, Ikkei Shikano, Michelle Peiffer, Asher G. Jones, Dawn S. Luthe, Kelli Hoover, and Gary W. Felton. "Plant defenses interact with insect enteric bacteria by initiating a leaky gut syndrome." Proceedings of the National Academy of Sciences 116, no. 32 (July 22, 2019): 15991–96. http://dx.doi.org/10.1073/pnas.1908748116.

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Plants produce suites of defenses that can collectively deter and reduce herbivory. Many defenses target the insect digestive system, with some altering the protective peritrophic matrix (PM) and causing increased permeability. The PM is responsible for multiple digestive functions, including reducing infections from potential pathogenic microbes. In our study, we developed axenic and gnotobiotic methods for fall armyworm (Spodoptera frugiperda) and tested how particular members present in the gut community influence interactions with plant defenses that can alter PM permeability. We observed interactions between gut bacteria with plant resistance. Axenic insects grew more but displayed lower immune-based responses compared with those possessing Enterococcus, Klebsiella, and Enterobacter isolates from field-collected larvae. While gut bacteria reduced performance of larvae fed on plants, none of the isolates produced mortality when injected directly into the hemocoel. Our results strongly suggest that plant physical and chemical defenses not only act directly upon the insect, but also have some interplay with the herbivore’s microbiome. Combined direct and indirect, microbe-mediated assaults by maize defenses on the fall armyworm on the insect digestive and immune system reduced growth and elevated mortality in these insects. These results imply that plant–insect interactions should be considered in the context of potential mediation by the insect gut microbiome.

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Obrenovich, Mark, Hayden Jaworski, Tara Tadimalla, Adil Mistry, Lorraine Sykes, George Perry, and Robert Bonomo. "The Role of the Microbiota–Gut–Brain Axis and Antibiotics in ALS and Neurodegenerative Diseases." Microorganisms 8, no. 5 (May 23, 2020): 784. http://dx.doi.org/10.3390/microorganisms8050784.

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The human gut hosts a wide and diverse ecosystem of microorganisms termed the microbiota, which line the walls of the digestive tract and colon where they co-metabolize digestible and indigestible food to contribute a plethora of biochemical compounds with diverse biological functions. The influence gut microbes have on neurological processes is largely yet unexplored. However, recent data regarding the so-called leaky gut, leaky brain syndrome suggests a potential link between the gut microbiota, inflammation and host co-metabolism that may affect neuropathology both locally and distally from sites where microorganisms are found. The focus of this manuscript is to draw connection between the microbiota–gut–brain (MGB) axis, antibiotics and the use of “BUGS AS DRUGS” for neurodegenerative diseases, their treatment, diagnoses and management and to compare the effect of current and past pharmaceuticals and antibiotics for alternative mechanisms of action for brain and neuronal disorders, such as Alzheimer disease (AD), Amyotrophic Lateral Sclerosis (ALS), mood disorders, schizophrenia, autism spectrum disorders and others. It is a paradigm shift to suggest these diseases can be largely affected by unknown aspects of the microbiota. Therefore, a future exists for applying microbial, chemobiotic and chemotherapeutic approaches to enhance translational and personalized medical outcomes. Microbial modifying applications, such as CRISPR technology and recombinant DNA technology, among others, echo a theme in shifting paradigms, which involve the gut microbiota (GM) and mycobiota and will lead to potential gut-driven treatments for refractory neurologic diseases.

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Kobayashi, Takashi, Michihiro Iwaki, Atsushi Nakajima, Asako Nogami, and Masato Yoneda. "Current Research on the Pathogenesis of NAFLD/NASH and the Gut–Liver Axis: Gut Microbiota, Dysbiosis, and Leaky-Gut Syndrome." International Journal of Molecular Sciences 23, no. 19 (October 2, 2022): 11689. http://dx.doi.org/10.3390/ijms231911689.

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Global lifestyle changes have led to an increased incidence of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), requiring further in-depth research to understand the mechanisms and develop new therapeutic strategies. In particular, high-fat and high-fructose diets have been shown to increase intestinal permeability, which can expose the liver to endotoxins. Indeed, accumulating evidence points to a link between these liver diseases and the intestinal axis, including dysbiosis of the gut microbiome and leaky-gut syndrome. Here, we review the mechanisms contributing to these links between the liver and small intestine in the pathogenesis of NAFLD/NASH, focusing on the roles of intestinal microbiota and their metabolites to influence enzymes essential for proper liver metabolism and function. Advances in next-generation sequencing technology have facilitated analyses of the metagenome, providing new insights into the roles of the intestinal microbiota and their functions in physiological and pathological mechanisms. This review summarizes recent research linking the gut microbiome to liver diseases, offering new research directions to elucidate the detailed mechanisms and novel targets for treatment and prevention.

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Chancharoenthana, Wiwat, Asada Leelahavanichkul, Wassawon Ariyanon, Somratai Vadcharavivad, Suphasit Phatcharophaswattanakul, Supitcha Kamolratanakul, Pornsawan Leaungwutiwong, Weerapong Phumratanaprapin, and Polrat Wilairatana. "Leaky Gut Syndrome Is Associated with Endotoxemia and Serum (1→3)-β-D-Glucan in Severe Dengue Infection." Microorganisms 9, no. 11 (November 19, 2021): 2390. http://dx.doi.org/10.3390/microorganisms9112390.

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The hallmark of severe dengue infection is the increased vascular permeability and hemodynamic alteration that might be associated with an intestinal permeability defect. However, the mechanisms underlying the gastrointestinal-related symptoms of dengue are not well characterized. A prospective observational study was conducted on patients with dengue who were categorized according to: (i) febrile versus critical phase and (ii) hospitalized patients with versus without the warning signs to evaluate the gut barrier using lactulose-to-mannitol excretion ratio (LEMR). Serum endotoxins, (1→3)-β-D-glucan (BG), and inflammatory parameters were measured. A total of 48 and 38 patients were enrolled in febrile illness and critical phase, respectively, while 22 and 64 patients presented with or without the warning signs, respectively. At enrollment, a positive LEMR test was found in 20 patients (91%) with warning signs, regardless of phase of infection. Likewise, serum endotoxins and BG, the indirect biomarkers for leaky gut, prominently increased in patients who developed severe dengue when compared with the non-severe dengue (endotoxins, 399.1 versus 143.4 pg/mL (p < 0.0001); BG, 123 versus 73.8 pg/mL (p = 0.016)). Modest impaired intestinal permeability occurred in dengue patients, particularly those with warning signs, and were associated with endotoxemia and elevated BG. Thus, leaky gut syndrome might be associated with severity of dengue infection.

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Binienda, Agata, Agata Twardowska, Adam Makaro, and Maciej Salaga. "Dietary Carbohydrates and Lipids in the Pathogenesis of Leaky Gut Syndrome: An Overview." International Journal of Molecular Sciences 21, no. 21 (November 8, 2020): 8368. http://dx.doi.org/10.3390/ijms21218368.

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This review summarizes the recent knowledge on the effects of dietary carbohydrates and lipids on the pathophysiology of leaky gut syndrome (LGS). Alterations in intestinal barrier permeability may lead to serious gastrointestinal (GI) disorders. LGS is caused by intestinal hyperpermeability due to changes in the expression levels and functioning of tight junctions. The influence of dietary habits on intestinal physiology is clearly visible in incidence rates of intestinal diseases in industrial and developing countries. Diseases which are linked to intestinal hyperpermeability tend to localize to Westernized countries, where a diet rich in fats and refined carbohydrates predominates. Several studies suggest that fructose is one of the key carbohydrates involved in the regulation of the intestinal permeability and its overuse may cause harmful effects, such as tight junction protein dysfunction. On the other hand, short chain fatty acids (mainly butyrate) at appropriate concentrations may lead to the reduction of intestinal permeability, which is beneficial in LGS. However, long chain fatty acids, including n-3 and n-6 polyunsaturated fatty acids have unclear properties. Some of those behave as components untightening and tightening the intestinal membrane.

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Di Tommaso, Natalia, Antonio Gasbarrini, and Francesca Romana Ponziani. "Intestinal Barrier in Human Health and Disease." International Journal of Environmental Research and Public Health 18, no. 23 (December 6, 2021): 12836. http://dx.doi.org/10.3390/ijerph182312836.

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The intestinal mucosa provides a selective permeable barrier for nutrient absorption and protection from external factors. It consists of epithelial cells, immune cells and their secretions. The gut microbiota participates in regulating the integrity and function of the intestinal barrier in a homeostatic balance. Pathogens, xenobiotics and food can disrupt the intestinal barrier, promoting systemic inflammation and tissue damage. Genetic and immune factors predispose individuals to gut barrier dysfunction, and changes in the composition and function of the gut microbiota are central to this process. The progressive identification of these changes has led to the development of the concept of ‘leaky gut syndrome’ and ‘gut dysbiosis’, which underlie the relationship between intestinal barrier impairment, metabolic diseases and autoimmunity. Understanding the mechanisms underlying this process is an intriguing subject of research for the diagnosis and treatment of various intestinal and extraintestinal diseases.

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Portincasa, Piero, Leonilde Bonfrate, Mohamad Khalil, Maria De Angelis, Francesco Maria Calabrese, Mauro D’Amato, David Q. H. Wang, and Agostino Di Ciaula. "Intestinal Barrier and Permeability in Health, Obesity and NAFLD." Biomedicines 10, no. 1 (December 31, 2021): 83. http://dx.doi.org/10.3390/biomedicines10010083.

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The largest surface of the human body exposed to the external environment is the gut. At this level, the intestinal barrier includes luminal microbes, the mucin layer, gastrointestinal motility and secretion, enterocytes, immune cells, gut vascular barrier, and liver barrier. A healthy intestinal barrier is characterized by the selective permeability of nutrients, metabolites, water, and bacterial products, and processes are governed by cellular, neural, immune, and hormonal factors. Disrupted gut permeability (leaky gut syndrome) can represent a predisposing or aggravating condition in obesity and the metabolically associated liver steatosis (nonalcoholic fatty liver disease, NAFLD). In what follows, we describe the morphological-functional features of the intestinal barrier, the role of major modifiers of the intestinal barrier, and discuss the recent evidence pointing to the key role of intestinal permeability in obesity/NAFLD.

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Croci, Sonia, Lina Ilaras D’Apolito, Valeria Gasperi, Maria Valeria Catani, and Isabella Savini. "Dietary Strategies for Management of Metabolic Syndrome: Role of Gut Microbiota Metabolites." Nutrients 13, no. 5 (April 21, 2021): 1389. http://dx.doi.org/10.3390/nu13051389.

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Metabolic syndrome (MetS) is a complex pathophysiological state with incidence similar to that of a global epidemic and represents a risk factor for the onset of chronic non-communicable degenerative diseases (NCDDs), including cardiovascular disease (CVD), type 2 diabetes mellitus, chronic kidney disease, and some types of cancer. A plethora of literature data suggest the potential role of gut microbiota in interfering with the host metabolism, thus influencing several MetS risk factors. Perturbation of the gut microbiota’s composition and activity, a condition known as dysbiosis, is involved in the etiopathogenesis of multiple chronic diseases. Recent studies have shown that some micro-organism-derived metabolites (including trimethylamine N-oxide (TMAO), lipopolysaccharide (LPS) of Gram-negative bacteria, indoxyl sulfate and p-cresol sulfate) induce subclinical inflammatory processes involved in MetS. Gut microbiota’s taxonomic species or abundance are modified by many factors, including diet, lifestyle and medications. The main purpose of this review is to highlight the correlation between different dietary strategies and changes in gut microbiota metabolites. We mainly focus on the validity/inadequacy of specific dietary patterns to reduce inflammatory processes, including leaky gut and subsequent endotoxemia. We also describe the chance of probiotic supplementation to interact with the immune system and limit negative consequences associated with MetS.

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Bartochowski, Piotr, Nathalie Gayrard, Stéphanie Bornes, Céline Druart, Angel Argilés, Magali Cordaillat-Simmons, and Flore Duranton. "Gut–Kidney Axis Investigations in Animal Models of Chronic Kidney Disease." Toxins 14, no. 9 (September 7, 2022): 626. http://dx.doi.org/10.3390/toxins14090626.

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Chronic kidney disease (CKD) is an incurable disease in which renal function gradually declines, resulting in no noticeable symptoms during the early stages and a life-threatening disorder in the latest stage. The changes that accompany renal failure are likely to influence the gut microbiota, or the ecosystem of micro-organisms resident in the intestine. Altered gut microbiota can display metabolic changes and become harmful to the host. To study the gut–kidney axis in vivo, animal models should ideally reproduce the disorders affecting both the host and the gut microbiota. Murine models of CKD, but not dog, manifest slowed gut transit, similarly to patient. Animal models of CKD also reproduce altered intestinal barrier function, as well as the resulting leaky gut syndrome and bacterial translocation. CKD animal models replicate metabolic but not compositional changes in the gut microbiota. Researchers investigating the gut–kidney axis should pay attention to the selection of the animal model (disease induction method, species) and the setting of the experimental design (control group, sterilization method, individually ventilated cages) that have been shown to influence gut microbiota.

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Gecse, Krisztina, Richárd Róka, Teréz Séra, András Rosztóczy, Anita Annaházi, Ferenc Izbéki, Ferenc Nagy, et al. "Leaky Gut in Patients with Diarrhea-Predominant Irritable Bowel Syndrome and Inactive Ulcerative Colitis." Digestion 85, no. 1 (2012): 40–46. http://dx.doi.org/10.1159/000333083.

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Kessoku, Takaomi, Takashi Kobayashi, Kosuke Tanaka, Atsushi Yamamoto, Kota Takahashi, Michihiro Iwaki, Anna Ozaki, et al. "The Role of Leaky Gut in Nonalcoholic Fatty Liver Disease: A Novel Therapeutic Target." International Journal of Molecular Sciences 22, no. 15 (July 29, 2021): 8161. http://dx.doi.org/10.3390/ijms22158161.

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The liver directly accepts blood from the gut and is, therefore, exposed to intestinal bacteria. Recent studies have demonstrated a relationship between gut bacteria and nonalcoholic fatty liver disease (NAFLD). Approximately 10–20% of NAFLD patients develop nonalcoholic steatohepatitis (NASH), and endotoxins produced by Gram-negative bacilli may be involved in NAFLD pathogenesis. NAFLD hyperendotoxicemia has intestinal and hepatic factors. The intestinal factors include impaired intestinal barrier function (leaky gut syndrome) and dysbiosis due to increased abundance of ethanol-producing bacteria, which can change endogenous alcohol concentrations. The hepatic factors include hyperleptinemia, which is associated with an excessive response to endotoxins, leading to intrahepatic inflammation and fibrosis. Clinically, the relationship between gut bacteria and NAFLD has been targeted in some randomized controlled trials of probiotics and other agents, but the results have been inconsistent. A recent randomized, placebo-controlled study explored the utility of lubiprostone, a treatment for constipation, in restoring intestinal barrier function and improving the outcomes of NAFLD patients, marking a new phase in the development of novel therapies targeting the intestinal barrier. This review summarizes recent data from studies in animal models and randomized clinical trials on the role of the gut–liver axis in NAFLD pathogenesis and progression.

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Miousse, Isabelle R., Laura E. Ewing, Charles M. Skinner, Rupak Pathak, Sarita Garg, Kristy R. Kutanzi, Stepan Melnyk, Martin Hauer-Jensen, and Igor Koturbash. "Methionine dietary supplementation potentiates ionizing radiation-induced gastrointestinal syndrome." American Journal of Physiology-Gastrointestinal and Liver Physiology 318, no. 3 (March 1, 2020): G439—G450. http://dx.doi.org/10.1152/ajpgi.00351.2019.

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Methionine is an essential amino acid needed for a variety of processes in living organisms. Ionizing radiation depletes tissue methionine concentrations and leads to the loss of DNA methylation and decreased synthesis of glutathione. In this study, we aimed to investigate the effects of methionine dietary supplementation in CBA/CaJ mice after exposure to doses ranging from 3 to 8.5 Gy of 137Cs of total body irradiation. We report that mice fed a methionine-supplemented diet (MSD; 19.5 vs. 6.5 mg/kg in a methionine-adequate diet, MAD) developed acute radiation toxicity at doses as low as 3 Gy. Partial body irradiation performed with hindlimb shielding resulted in a 50% mortality rate in MSD-fed mice exposed to 8.5 Gy, suggesting prevalence of radiation-induced gastrointestinal syndrome in the development of acute radiation toxicity. Analysis of the intestinal microbiome demonstrated shifts in the gut ecology, observed along with the development of leaky gut syndrome and bacterial translocation into the liver. Normal gut physiology impairment was facilitated by alterations in the one-carbon metabolism pathway and was exhibited as decreases in circulating citrulline levels mirrored by decreased intestinal mucosal surface area and the number of surviving crypts. In conclusion, we demonstrate that a relevant excess of methionine dietary intake exacerbates the detrimental effects of exposure to ionizing radiation in the small intestine. NEW & NOTEWORTHY Methionine supplementation, instead of an anticipated health-promoting effect, sensitizes mice to gastrointestinal radiation syndrome. Mechanistically, excess of methionine negatively affects intestinal ecology, leading to a cascade of physiological, biochemical, and molecular alterations that impair normal gut response to a clinically relevant genotoxic stressor. These findings speak toward increasing the role of registered dietitians during cancer therapy and the necessity of a solid scientific background behind the sales of dietary supplements and claims regarding their benefits.

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Polak, Karina, Beata Bergler-Czop, Michał Szczepanek, Kamila Wojciechowska, Aleksandra Frątczak, and Norbert Kiss. "Psoriasis and Gut Microbiome—Current State of Art." International Journal of Molecular Sciences 22, no. 9 (April 26, 2021): 4529. http://dx.doi.org/10.3390/ijms22094529.

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Psoriasis is a chronic, immune-mediated inflammatory disease that affects around 125 million people worldwide. Several studies concerning the gut microbiota composition and its role in disease pathogenesis recently demonstrated significant alterations among psoriatic patients. Certain parameters such as Firmicutes/Bacteroidetes ratio or Psoriasis Microbiome Index were developed in order to distinguish between psoriatic and healthy individuals. The “leaky gut syndrome” and bacterial translocation is considered by some authors as a triggering factor for the onset of the disease, as it promotes chronic systemic inflammation. The alterations were also found to resemble those in inflammatory bowel diseases, obesity and certain cardiovascular diseases. Microbiota dysbiosis, depletion in SCFAs production, increased amount of produced TMAO, dysregulation of the pathways affecting the balance between lymphocytes populations seem to be the most significant findings concerning gut physiology in psoriatic patients. The gut microbiota may serve as a potential response-to-treatment biomarker in certain cases of biological treatment. Oral probiotics administration as well as fecal microbial transplantation were most reported in bringing health benefits to psoriatic patients. However, the issue of psoriatic bacterial gut composition, its role and healing potential needs further investigation. Here we reviewed the literature on the current state of the relationship between psoriasis and gut microbiome.

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Wu, Chia-Shan, Jiyeon Noh, Ellie Tuchaai, Jennifer A. DeLuca, Kimberly F. Allred, Clinton D. Allred, and Yuxiang Sun. "SUPPRESSION OF GHRELIN SIGNALING EXACERBATES ULCERATIVE COLITIS IN OLDER MICE." Innovation in Aging 3, Supplement_1 (November 2019): S87. http://dx.doi.org/10.1093/geroni/igz038.334.

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Abstract The aging process is characterized by increased chronic low-grade inflammation, aka inflamm-aging, which offend is accompanied by ‘leaky gut’ syndrome. Inflamm-aging is a highly significant risk factor for both morbidity and mortality in the older adult population (>65 years of age). In addition, there is a growing prevalence of inflammatory bowel disease (IBD), a chronic inflammatory condition of the gastrointestinal tract in the older adult population. The pathogenesis of late-onset IBD is suggested to be more complex compared with younger IBD patients; the causes determining the age of IBD onset remain unexplained. Ghrelin is a 28-amino-acid peptide hormone mainly produced by X/A-like cells of the stomach, with well-characterized functions in growth hormone secretion, food intake, adiposity and insulin resistance. Ghrelin’s biological relevant receptor is Growth Hormone Secretagogue Receptor (GHS-R). Ghrelin and ghrelin mimetics have been considered viable candidates for treating cachexia, sarcopenia, and gastrointestinal disorders. As expected, we observed that the expression of tight junction proteins in colon mucosal layer decreases with age. When challenged with dextran sulfate sodium (DSS) to induce experimental ulcerative colitis, 18-months old male C57BL/6 mice exhibited exacerbated disease activity scores compared to young male mice (5-months), showing worsened pathology such as rectal bleeding and difficulty in defecation. DSS-induced colitis was exacerbated in both ghrelin-deficient (Ghrl-/-) and ghrelin receptor-deficient (Ghsr-/-) mice. Together, these data suggest endogenous ghrelin signaling contributes to susceptibility to colitis, and ghrelin signaling pathway may present a novel target for prevention and treatment of leaky gut syndrome in aging.

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Santos, Gilberto Maia, Shámila Ismael, Juliana Morais, João R. Araújo, Ana Faria, Conceição Calhau, and Cláudia Marques. "Intestinal Alkaline Phosphatase: A Review of This Enzyme Role in the Intestinal Barrier Function." Microorganisms 10, no. 4 (March 30, 2022): 746. http://dx.doi.org/10.3390/microorganisms10040746.

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Intestinal alkaline phosphatase (IALP) has recently assumed a special relevance, being the subject of study in the prevention and treatment of certain diseases related to leaky gut. This brush border enzyme (ecto-enzyme) plays an important role in the maintenance of intestinal microbial homeostasis and intestinal barrier function through its ability to dephosphorylate lipopolysaccharide (LPS). This review addresses how IALP and intestinal barrier dysfunction may be implicated in the pathophysiology of specific diseases such as inflammatory bowel disease, necrotizing enterocolitis, and metabolic syndrome. The use of IALP as a possible biomarker to assess intestinal barrier function and strategies to modulate IALP activity are also discussed.

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Ukrainets, R. V., and Yu S. Korneva. "Epithelial-mesenchimal transition and its relationship with leaky gut syndrome as possible step in pathogenesis of endometriosis." Problemy reproduktsii 26, no. 5 (2020): 133. http://dx.doi.org/10.17116/repro202026051133.

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Lee, Sang-Hoon, and Sang Man Kim. "Functional medical approach to food intolerance." Korean Institute for Functional Medicine 5, no. 2 (November 30, 2022): 10–17. http://dx.doi.org/10.32581/jkifm.2022.5.2.10.

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Food intolerances are defined as difficulty digesting or metabolizing a particular food. They are a subset of adverse food reactions. Adverse food reactions include immune-mediated food allergies and non-immune-mediated food intolerances. Food intolerances are estimated to affect up to 15-20% of the population, but understanding of diagnosis and management is complicated and controversial, and given presentation and mechanisms associated also vary greatly. In addition, food intolerances can be associated with various clinical imbalances of functional medicine, such as dysbiosis, leaky gut syndrome, histamine imbalance, and functional adrenal insufficiency. This review aims to provide a scientific update and clinical application of food intolerances in the perspective of functional medicine.

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Rushing, Blake, Susan McRitchie, Liubov Arbeeva, Amanda Nelson, M. Andrea Azcarate-Peril, Yuan-Yuan Li, Yunzhi Qian, Susan Sumner, and Richard Loeser. "Untargeted Fecal Metabolomics to Investigate the Role of the Microbiome and Nutrients in Osteoarthritis." Current Developments in Nutrition 5, Supplement_2 (June 2021): 47. http://dx.doi.org/10.1093/cdn/nzab033_047.

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Abstract Objectives The objective of this study was to determine if perturbations in gut microbial composition and the gut metabolome could be linked to individuals with obesity and osteoarthritis (OA). Methods Fecal samples were collected from 92 participants with obesity recruited from the Johnston County Osteoarthritis Project. OA cases (n = 59) had radiographic hand plus knee OA, defined as involvement of at least 3 joints across both hands, and a Kellgren-Lawrence (KL) grade 2–4 in at least one knee. Controls (n = 33) were without hand OA and with KL grade 0–1 knees. Fecal metabolomes were analyzed by a UHPLC/Q Exactive HFx mass spectrometer. Microbiome composition was determined in fecal samples by 16S ribosomal RNA amplicon sequencing (rRNA-seq). Stepwise logistic regression models were built to determine predictors of OA status. Spearman correlations were performed to determine associations between metabolites and microbiota in OA or healthy individuals. Results Untargeted metabolomics analysis indicated that OA cases had significantly higher levels of di- and tri-peptides (P < 0.05), and significant perturbations (P < 0.1) in microbial metabolites. Pathway analysis revealed several significantly perturbed pathways (P < 0.05) associated with OA, including leukotriene metabolism, amino acid metabolism and fatty acid utilization. Logistic regression models selected metabolites associated with the microbiota and leaky gut syndrome as significant predictors of OA status, particularly when combined with the 16S rRNA sequencing data. Omega-3/6 polyunsaturated fatty acids (PUFAs) levels were significantly correlated with the phyla Bacteriodetes and Firmicutes. Conclusions Adults with obesity and OA have distinct fecal metabolomes characterized by perturbations in microbial metabolites, PUFAs, and protein digestion compared with healthy controls. These metabolic perturbations suggest a role of intestinal inflammation and leaky gut in OA. Funding Sources Supported by the Arthritis Foundation, the National Center for Advancing Translational Sciences (NCATS) (UL1TR002489), and the National Institute of Arthritis and Musculoskeletal and Skin Diseases (P30AR072580).

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La Rosa, Francesca, Mario Clerici, Daniela Ratto, Alessandra Occhinegro, Anna Licito, Marcello Romeo, Carmine Iorio, and Paola Rossi. "The Gut-Brain Axis in Alzheimer’s Disease and Omega-3. A Critical Overview of Clinical Trials." Nutrients 10, no. 9 (September 8, 2018): 1267. http://dx.doi.org/10.3390/nu10091267.

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Despite intensive study, neurodegenerative diseases remain insufficiently understood, precluding rational design of therapeutic interventions that can reverse or even arrest the progressive loss of neurological function. In the last decade, several theories investigating the causes of neurodegenerative diseases have been formulated and a condition or risk factor that can contribute is described by the gut-brain axis hypothesis: stress, unbalanced diet, and drugs impact altering microbiota composition which contributes to dysbiosis. An altered gut microbiota may lead to a dysbiotic condition and to a subsequent increase in intestinal permeability, causing the so-called leaky-gut syndrome. Herein, in this review we report recent findings in clinical trials on the risk factor of the gut-brain axis in Alzheimer’s disease and on the effect of omega-3 supplementation, in shifting gut microbiota balance towards an eubiosis status. Despite this promising effect, evidences reported in selected randomized clinical trials on the effect of omega-3 fatty acid on cognitive decline in Alzheimer’s disease are few. Only Mild Cognitive Impairment, a prodromal state that could precede the progress to Alzheimer’s disease could be affected by omega-3 FA supplementation. We report some of the critical issues which emerged from these studies. Randomized controlled trials in well-selected AD patients considering the critical points underlined in this review are warranted.

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Wada, Koichiro, Haruki Usuda, Takayuki Okamoto, and Tomomi Niibayashi. "Increased permeability of intestinal mucosa and multi-organ association: Leaky Gut Syndrome as a target for drug discovery." Proceedings for Annual Meeting of The Japanese Pharmacological Society 95 (2022): 1—S06–4. http://dx.doi.org/10.1254/jpssuppl.95.0_1-s06-4.

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Usuda, Haruki, Tomomi Niibayashi, Tetsuya Tanaka, Takayuki Okamoto, and Koichiro Wada. "Novel method for evaluating leaky gut syndrome induced by NSAIDs/PPI and ischemia with health food-derived reagents." Proceedings for Annual Meeting of The Japanese Pharmacological Society WCP2018 (2018): PO3–5–19. http://dx.doi.org/10.1254/jpssuppl.wcp2018.0_po3-5-19.

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Basiouni, Shereen, Guillermo Tellez-Isaias, Juan D. Latorre, Brittany D. Graham, Victor M. Petrone-Garcia, Hesham R. El-Seedi, Sakine Yalçın, et al. "Anti-Inflammatory and Antioxidative Phytogenic Substances against Secret Killers in Poultry: Current Status and Prospects." Veterinary Sciences 10, no. 1 (January 14, 2023): 55. http://dx.doi.org/10.3390/vetsci10010055.

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Chronic stress is recognized as a secret killer in poultry. It is associated with systemic inflammation due to cytokine release, dysbiosis, and the so-called leaky gut syndrome, which mainly results from oxidative stress reactions that damage the barrier function of the cells lining the gut wall. Poultry, especially the genetically selected broiler breeds, frequently suffer from these chronic stress symptoms when exposed to multiple stressors in their growing environments. Since oxidative stress reactions and inflammatory damages are multi-stage and long-term processes, overshooting immune reactions and their down-stream effects also negatively affect the animal’s microbiota, and finally impair its performance and commercial value. Means to counteract oxidative stress in poultry and other animals are, therefore, highly welcome. Many phytogenic substances, including flavonoids and phenolic compounds, are known to exert anti-inflammatory and antioxidant effects. In this review, firstly, the main stressors in poultry, such as heat stress, mycotoxins, dysbiosis and diets that contain oxidized lipids that trigger oxidative stress and inflammation, are discussed, along with the key transcription factors involved in the related signal transduction pathways. Secondly, the most promising phytogenic substances and their current applications to ameliorate oxidative stress and inflammation in poultry are highlighted.

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Peruhova, Milena, Antoaneta Mihova, Iskra Altankova, and Tsvetelina Velikova. "Specific Immunoglobulin E and G to Common Food Antigens and Increased Serum Zonulin in IBS Patients: A Single-Center Bulgarian Study." Antibodies 11, no. 2 (March 29, 2022): 23. http://dx.doi.org/10.3390/antib11020023.

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Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder whose pathogenesis is considered multifactorial, including abnormal gut motility, visceral hyperreactivity, psychological factors, disturbances in the brain-gut axis, leaky gut, oxidative stress, etc. We aimed to investigate serum levels of specific immunoglobulin E and G to common food antigens and zonulin and to assess their use in clinical practice for patients with IBS. Material and methods. We included 23 participants, 15 with IBS (diagnosed according to the Rome IV criteria) and 8 healthy controls. We investigated serum levels of specific IgG antibodies to 24 food antigens, specific IgE antibodies to 20 food antigens, anti-celiac antibodies, fecal calprotectin and serum zonulin by ELISA. Results. Food-specific positive IgG antibodies were significantly higher in patients with IBS than in controls (p = 0.007). IgE-mediated allergic reactions were found in five patients with IBS; no one had anti-TG antibodies. One-third of IBS patients demonstrated a low degree of chronic inflammation (positive fecal calprotectin test > 50 ng/mL) without specific bacterial infection. Serum levels of zonulin in IBS patients were higher than in healthy controls (0.378 ± 0.13 vs. 0.250 ± 0.14 ng/mL, p = 0.0315). However, no correlations between clinical symptoms and zonulin levels were found. Conclusion. The mechanisms of IgG hypersensitivity and low degree inflammation in IBS and elevated zonulin may contribute to multifactor pathogenesis in IBS.

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Shehata, Awad A., Youssef Attia, Asmaa F. Khafaga, Muhammad Z. Farooq, Hesham R. El-Seedi, Wolfgang Eisenreich, and Guillermo Tellez-Isaias. "Restoring healthy gut microbiome in poultry using alternative feed additives with particular attention to phytogenic substances: Challenges and prospects." German Journal of Veterinary Research 2, no. 3 (2022): 32–42. http://dx.doi.org/10.51585/gjvr.2022.3.0047.

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The majority of pathologies in poultry are linked to intestinal chronic inflammation due to a disbalance of the gut microbiota. Thus, a healthy microbiota drives the gut integrity, and the gut’s biological and metabolic functionalities, including efficacious use of nutrition, but also immunity, and neuroendocrine systems. However, many external factors are disturbing a stable, healthy gut microbiota. Heat stress, dysbiosis, leaky gut syndrome, and mycotoxins are the main “secret killers” in poultry that lead to chronic oxidative stress and inflammation, which in turn impact the health and animal performance. Additionally, chronic stress in poultry is linked with the emergence of antimicrobial resistance (AMR), which the WHO has recently identified to be among the most important problems threatening human health globally that increased the demand for safe antimicrobials to treat the collateral damages resulting from dysbiosis. Several alternative feed additives such as probiotics, prebiotics, fatty acids, and amino acids have been described to restore intestinal microbiota. Additionally, some phytogenic substances have anti-inflammatory and antioxidant activities. These natural products are also capable to modulate gut microbiota in a symbiotic equilibrium, thereby enabling the intestinal tract to withstand both infectious and non-infectious stressors. Nevertheless, several challenges, such as the bioavailability, rate of absorption, quality inconsistency, public acceptance, and cost-effective delivery methods, make the feasibility and application of phytogenic substances on a commercial scale complicated. In this review, the main drivers of chronic inflammation in poultry have been discussed. Additionally, the potential use of alternatives to antibiotics to restore the gastrointestinal microbiota in poultry and the possibilities for overcoming breakdowns in poultry farming were highlighted

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Plaza-Díaz, Julio, Patricio Solís-Urra, Fernando Rodríguez-Rodríguez, Jorge Olivares-Arancibia, Miguel Navarro-Oliveros, Francisco Abadía-Molina, and Ana I. Álvarez-Mercado. "The Gut Barrier, Intestinal Microbiota, and Liver Disease: Molecular Mechanisms and Strategies to Manage." International Journal of Molecular Sciences 21, no. 21 (November 7, 2020): 8351. http://dx.doi.org/10.3390/ijms21218351.

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Liver disease encompasses pathologies as non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, alcohol liver disease, hepatocellular carcinoma, viral hepatitis, and autoimmune hepatitis. Nowadays, underlying mechanisms associating gut permeability and liver disease development are not well understood, although evidence points to the involvement of intestinal microbiota and their metabolites. Animal studies have shown alterations in Toll-like receptor signaling related to the leaky gut syndrome by the action of bacterial lipopolysaccharide. In humans, modifications of the intestinal microbiota in intestinal permeability have also been related to liver disease. Some of these changes were observed in bacterial species belonging Roseburia, Streptococcus, and Rothia. Currently, numerous strategies to treat liver disease are being assessed. This review summarizes and discusses studies addressed to determine mechanisms associated with the microbiota able to alter the intestinal barrier complementing the progress and advancement of liver disease, as well as the main strategies under development to manage these pathologies. We highlight those approaches that have shown improvement in intestinal microbiota and barrier function, namely lifestyle changes (diet and physical activity) and probiotics intervention. Nevertheless, knowledge about how such modifications are beneficial is still limited and specific mechanisms involved are not clear. Thus, further in-vitro, animal, and human studies are needed.

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Gawlik-Kotelnicka, Oliwia, Aleksandra Margulska, Agata Gabryelska, Marcin Sochal, Piotr Białasiewicz, and Dominik Strzelecki. "“Leaky Gut” as a Keystone of the Connection between Depression and Obstructive Sleep Apnea Syndrome? A Rationale and Study Design." Metabolites 12, no. 2 (February 6, 2022): 152. http://dx.doi.org/10.3390/metabo12020152.

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Obstructive sleep apnea (OSA) and depression are highly comorbid. Immune alterations, oxidative stress or microbiota dysfunction have been proposed as some mechanisms underlying this association. The aim of the proposed study is to assess the severity and profile of OSA and depressive symptoms in the context of serum microbiota metabolites, biomarkers of intestinal permeability, inflammation and oxidative stress in adult patients diagnosed with OSA syndrome. The study population consists of 200 subjects. An apnoea-hypopnoea index ≥ 5/hour is used for the diagnosis. Depressive symptoms are assessed with Beck Depression Inventory. Measured serum markers are: tumour necrosis factor–alpha and interleukin-6 for inflammation, total antioxidant capacity and malondialdehyde concentration for oxidative stress, zonulin, calprotectin, lipopolisaccharide-binding protein and intestinal fatty acids-binding protein for intestinal permeability. All of the above will be measured by enzyme-linked immunosorbent assay (ELISA). Associations between clinical symptoms profile and severity and the above markers levels will be tested. It would be valuable to seek for overlap indicators of depression and OSA to create this endophenotype possible biomarkers and form new prophylactic or therapeutic methods. The results may be useful to establish a subpopulation of patients sensitive to microbiota therapeutic interventions (probiotics, prebiotics, and microbiota transplantation).

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Rahman-Enyart, Afrida, Wenbin Yang, Ryan E. Yaggie, Bryan A. White, Michael Welge, Loretta Auvil, Matthew Berry, et al. "Acyloxyacyl hydrolase is a host determinant of gut microbiome-mediated pelvic pain." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 321, no. 3 (September 1, 2021): R396—R412. http://dx.doi.org/10.1152/ajpregu.00106.2021.

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Dysbiosis of gut microbiota is associated with many pathologies, yet host factors modulating microbiota remain unclear. Interstitial cystitis/bladder pain syndrome (IC/BPS) is a debilitating condition of chronic pelvic pain often with comorbid urinary dysfunction and anxiety/depression, and recent studies find fecal dysbiosis in patients with IC/BPS. We identified the locus encoding acyloxyacyl hydrolase, Aoah, as a modulator of pelvic pain severity in a murine IC/BPS model. AOAH-deficient mice spontaneously develop rodent correlates of pelvic pain, increased responses to induced pelvic pain models, voiding dysfunction, and anxious/depressive behaviors. Here, we report that AOAH-deficient mice exhibit dysbiosis of gastrointestinal (GI) microbiota. AOAH-deficient mice exhibit an enlarged cecum, a phenotype long associated with germ-free rodents, and a “leaky gut” phenotype. AOAH-deficient ceca showed altered gene expression consistent with inflammation, Wnt signaling, and urologic disease. 16S sequencing of stool revealed altered microbiota in AOAH-deficient mice, and GC-MS identified altered metabolomes. Cohousing AOAH-deficient mice with wild-type mice resulted in converged microbiota and altered predicted metagenomes. Cohousing also abrogated the pelvic pain phenotype of AOAH-deficient mice, which was corroborated by oral gavage of AOAH-deficient mice with stool slurry of wild-type mice. Converged microbiota also alleviated comorbid anxiety-like behavior in AOAH-deficient mice. Oral gavage of AOAH-deficient mice with anaerobes cultured from IC/BPS stool resulted in exacerbation of pelvic allodynia. Together, these data indicate that AOAH is a host determinant of normal gut microbiota, and dysbiosis associated with AOAH deficiency contributes to pelvic pain. These findings suggest that the gut microbiome is a potential therapeutic target for IC/BPS.

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Belyakov, D. G., O. V. Gaus, and D. A. Gavrilenko. "Mucosal barrier role in the formation of irritable bowel syndrome as a potential target for disease therapy." Russian Medical Inquiry 6, no. 8 (2022): 458–63. http://dx.doi.org/10.32364/2587-6821-2022-6-8-458-463.

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Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorders, significantly reducing the life quality of patients and negatively affecting public health in general. For a long period of time, this pathology has been studied exclusively from the view of gastrointestinal motility disorder and visceral hypersensitivity. At the same time, there is more and more evidence that a significant role in the disease pathogenesis can be played by the intestinal epithelial barrier dysfunction It has been established that the penetration of antigens from the intestinal lumen into the internal environment can contribute to excessive antigenic stimulation and the low degree inflammation in the intestinal mucosa, characteristic of IBS. In recent years, a huge number of studies have been devoted to the research concerning the phenomenon of "increased intestinal permeability" and the search for targeted molecules for pathogenetic therapy of IBS, a brief overview of which is presented in this article. Correction of dysbiotic disorders through the use of pro-, pre- and synbiotics, fecal transplantation and enhanced resistance of the intestinal mucosa by prescribing cytoprotectors seems promising KEYWORDS: mucosal barrier, irritable bowel syndrome, increased intestinal permeability, leaky gut syndrome, probiotics, prebiotics. FOR CITATION: Belyakov D.G., Gaus O.V., Gavrilenko D.A. Mucosal barrier role in the formation of irritable bowel syndrome as a potential target for disease therapy. Russian Medical Inquiry. 2022;6(8):458–463 (in Russ.). DOI: 10.32364/2587-6821-2022-6-8-458-463.

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Journal articles on the topic 'Leaky-gut syndrome'

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