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Journal articles on the topic 'Neuro-immune diseases'
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1
Kerschensteiner, M., E. Meinl, and R. Hohlfeld. "Neuro-immune crosstalk in CNS diseases." Neuroscience 158, no. 3 (2009): 1122–32. http://dx.doi.org/10.1016/j.neuroscience.2008.09.009.
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Morris, Gerwyn, Michael Berk, Piotr Galecki, Ken Walder, and Michael Maes. "The Neuro-Immune Pathophysiology of Central and Peripheral Fatigue in Systemic Immune-Inflammatory and Neuro-Immune Diseases." Molecular Neurobiology 53, no. 2 (2015): 1195–219. http://dx.doi.org/10.1007/s12035-015-9090-9.
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He, Cuiying, Qian Wang, Jinyan Gao, Hongbing Chen, and Ping Tong. "Neuro-immune regulation in allergic Diseases: Role of neuropeptides." International Immunopharmacology 145 (January 2025): 113771. https://doi.org/10.1016/j.intimp.2024.113771.
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Camp, Belinda, Sabine Stegemann-Koniszewski, and Jens Schreiber. "Infection-Associated Mechanisms of Neuro-Inflammation and Neuro-Immune Crosstalk in Chronic Respiratory Diseases." International Journal of Molecular Sciences 22, no. 11 (2021): 5699. http://dx.doi.org/10.3390/ijms22115699.
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Chronic obstructive airway diseases are characterized by airflow obstruction and airflow limitation as well as chronic airway inflammation. Especially bronchial asthma and chronic obstructive pulmonary disease (COPD) cause considerable morbidity and mortality worldwide, can be difficult to treat, and ultimately lack cures. While there are substantial knowledge gaps with respect to disease pathophysiology, our awareness of the role of neurological and neuro-immunological processes in the development of symptoms, the progression, and the outcome of these chronic obstructive respiratory diseases, is growing. Likewise, the role of pathogenic and colonizing microorganisms of the respiratory tract in the development and manifestation of asthma and COPD is increasingly appreciated. However, their role remains poorly understood with respect to the underlying mechanisms. Common bacteria and viruses causing respiratory infections and exacerbations of chronic obstructive respiratory diseases have also been implicated to affect the local neuro-immune crosstalk. In this review, we provide an overview of previously described neuro-immune interactions in asthma, COPD, and respiratory infections that support the hypothesis of a neuro-immunological component in the interplay between chronic obstructive respiratory diseases, respiratory infections, and respiratory microbial colonization.
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Reale, Marcella, and Erica Costantini. "Cholinergic Modulation of the Immune System in Neuroinflammatory Diseases." Diseases 9, no. 2 (2021): 29. http://dx.doi.org/10.3390/diseases9020029.
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Frequent diseases of the CNS, such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and psychiatric disorders (e.g., schizophrenia), elicit a neuroinflammatory response that contributes to the neurodegenerative disease process itself. The immune and nervous systems use the same mediators, receptors, and cells to regulate the immune and nervous systems as well as neuro-immune interactions. In various neurodegenerative diseases, peripheral inflammatory mediators and infiltrating immune cells from the periphery cause exacerbation to current injury in the brain. Acetylcholine (ACh) plays a crucial role in the peripheral and central nervous systems, in fact, other than cells of the CNS, the peripheral immune cells also possess a cholinergic system. The findings on peripheral cholinergic signaling, and the activation of the “cholinergic anti-inflammatory pathway” mediated by ACh binding to α7 nAChR as one of the possible mechanisms for controlling inflammation, have restarted interest in cholinergic-mediated pathological processes and in the new potential therapeutic target for neuro-inflammatory-degenerative diseases. Herein, we focus on recent progress in the modulatory mechanisms of the cholinergic anti-inflammatory pathway in neuroinflammatory diseases.
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Chu, Coco, David Artis, and Isaac M. Chiu. "Neuro-immune Interactions in the Tissues." Immunity 52, no. 3 (2020): 464–74. http://dx.doi.org/10.1016/j.immuni.2020.02.017.
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Voisin, Tiphaine, Amélie Bouvier, and Isaac M. Chiu. "Neuro-immune interactions in allergic diseases: novel targets for therapeutics." International Immunology 29, no. 6 (2017): 247–61. http://dx.doi.org/10.1093/intimm/dxx040.
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Bjørklund, Geir, Lili Zou, Massimiliano Peana, et al. "The Role of the Thioredoxin System in Brain Diseases." Antioxidants 11, no. 11 (2022): 2161. http://dx.doi.org/10.3390/antiox11112161.
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The thioredoxin system, consisting of thioredoxin (Trx), thioredoxin reductase (TrxR), and NADPH, plays a fundamental role in the control of antioxidant defenses, cell proliferation, redox states, and apoptosis. Aberrations in the Trx system may lead to increased oxidative stress toxicity and neurodegenerative processes. This study reviews the role of the Trx system in the pathophysiology and treatment of Alzheimer’s, Parkinson’s and Huntington’s diseases, brain stroke, and multiple sclerosis. Trx system plays an important role in the pathophysiology of those disorders via multiple interactions through oxidative stress, apoptotic, neuro-immune, and pro-survival pathways. Multiple aberrations in Trx and TrxR systems related to other redox systems and their multiple reciprocal relationships with the neurodegenerative, neuro-inflammatory, and neuro-oxidative pathways are here analyzed. Genetic and environmental factors (nutrition, metals, and toxins) may impact the function of the Trx system, thereby contributing to neuropsychiatric disease. Aberrations in the Trx and TrxR systems could be a promising drug target to prevent and treat neurodegenerative, neuro-inflammatory, neuro-oxidative stress processes, and related brain disorders.
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Vojvodic, Aleksandra, Zorica Peric-Hajzler, Dusica Matovic, et al. "Gut Microbiota and the Alteration of Immune Balance in Skin Diseases: From Nutraceuticals to Fecal Transplantation." Open Access Macedonian Journal of Medical Sciences 7, no. 18 (2019): 3034–38. http://dx.doi.org/10.3889/oamjms.2019.827.
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T
 The P.N.E.I. (Psycho-Neuro-Endocrine-Immunology) approach is represented by the interdisciplinary concept of bidirectional cross-talk between the psycho-neuro-endocrine and immune systems, which can influence the immune response. The well-known Gut-Brain Axis and the Gut-Skin Axis can be merged in a bigger network- the Gut-Brain-Skin Axis, with complex regulation by cytokines, neuro-peptides, neuro-hormones and another messenger (signalling) molecules and maybe the most important modulator of the Gut-Brain-Skin Axis/ the gut microbiota. The role of gut bacterial homeostasis is very important, and the homeostatic imbalance of the immune response may be a relevant etiologic/pathophysiologic factor for extra-intestinal and intestinal inflammatory, allergic and autoimmune diseases. The Low Dose Cytokines Medicine (LDM) is an innovative therapeutic approach. It is based on the most advanced knowledge in molecular biology and low dose pharmacology with the primary outcome. The SKA (Sequential Kinetic Activation) technology, codified and standardised by GUNA S.p.a. -Italy- makes the low doses of signalling molecules able to be active even below the minimum dose classically considered as effective and the significative efficacy of orally administered low-dose signalling molecules is the most representative aspect of LDM. The Physiologic Nutraceuticals and the Low Dose Medicine are two of the most promising approaches for the treatment of skin diseases based on the rebalance of the immune response and the recovery of gut dysbiosis.
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Deczkowska, Aleksandra, and Michal Schwartz. "Targeting neuro–immune communication in neurodegeneration: Challenges and opportunities." Journal of Experimental Medicine 215, no. 11 (2018): 2702–4. http://dx.doi.org/10.1084/jem.20181737.
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Immune cells patrol the brain and can support its function, but can we modulate brain–immune communication to fight neurological diseases? Here, we briefly discuss the mechanisms orchestrating the cross-talk between the brain and the immune system and describe how targeting this interaction in a well-controlled manner could be developed as a universal therapeutic approach to treat neurodegeneration.
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Jacobson, Amanda, Daping Yang, Madeleine Vella, and Isaac M. Chiu. "The intestinal neuro-immune axis: crosstalk between neurons, immune cells, and microbes." Mucosal Immunology 14, no. 3 (2021): 555–65. http://dx.doi.org/10.1038/s41385-020-00368-1.
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AbstractThe gastrointestinal tract is densely innervated by a complex network of neurons that coordinate critical physiological functions. Here, we summarize recent studies investigating the crosstalk between gut-innervating neurons, resident immune cells, and epithelial cells at homeostasis and during infection, food allergy, and inflammatory bowel disease. We introduce the neuroanatomy of the gastrointestinal tract, detailing gut-extrinsic neuron populations from the spinal cord and brain stem, and neurons of the intrinsic enteric nervous system. We highlight the roles these neurons play in regulating the functions of innate immune cells, adaptive immune cells, and intestinal epithelial cells. We discuss the consequences of such signaling for mucosal immunity. Finally, we discuss how the intestinal microbiota is integrated into the neuro-immune axis by tuning neuronal and immune interactions. Understanding the molecular events governing the intestinal neuro-immune signaling axes will enhance our knowledge of physiology and may provide novel therapeutic targets to treat inflammatory diseases.
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Wang, Tianshu, Hailing Duan, Javier Santos, et al. "Intelligent treatment system based on bioinformatics and neuro-immune-digestive tract diseases." Alexandria Engineering Journal 107 (November 2024): 415–33. http://dx.doi.org/10.1016/j.aej.2024.07.043.
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Beopoulos, Athanasios, Manuel Gea, Alessio Fasano, and François Iris. "Autonomic Nervous System Neuroanatomical Alterations Could Provoke and Maintain Gastrointestinal Dysbiosis in Autism Spectrum Disorder (ASD): A Novel Microbiome–Host Interaction Mechanistic Hypothesis." Nutrients 14, no. 1 (2021): 65. http://dx.doi.org/10.3390/nu14010065.
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Dysbiosis secondary to environmental factors, including dietary patterns, antibiotics use, pollution exposure, and other lifestyle factors, has been associated to many non-infective chronic inflammatory diseases. Autism spectrum disorder (ASD) is related to maternal inflammation, although there is no conclusive evidence that affected individuals suffer from systemic low-grade inflammation as in many psychological and psychiatric diseases. However, neuro-inflammation and neuro–immune abnormalities are observed within ASD-affected individuals. Rebalancing human gut microbiota to treat disease has been widely investigated with inconclusive and contradictory findings. These observations strongly suggest that the forms of dysbiosis encountered in ASD-affected individuals could also originate from autonomic nervous system (ANS) functioning abnormalities, a common neuro–anatomical alteration underlying ASD. According to this hypothesis, overactivation of the sympathetic branch of the ANS, due to the fact of an ASD-specific parasympathetic activity deficit, induces deregulation of the gut–brain axis, attenuating intestinal immune and osmotic homeostasis. This sets-up a dysbiotic state, that gives rise to immune and osmotic dysregulation, maintaining dysbiosis in a vicious cycle. Here, we explore the mechanisms whereby ANS imbalances could lead to alterations in intestinal microbiome–host interactions that may contribute to the severity of ASD by maintaining the brain–gut axis pathways in a dysregulated state.
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Ueno, Masaki. "Restoring neuro-immune circuitry after brain and spinal cord injuries." International Immunology 33, no. 6 (2021): 311–25. http://dx.doi.org/10.1093/intimm/dxab017.
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Abstract Neuro-immune interactions are essential for our body’s defense and homeostasis. Anatomical and physiological analyses have shown that the nervous system comprises multiple pathways that regulate the dynamics and functions of immune cells, which are mainly mediated by the autonomic nervous system and adrenal signals. These are disturbed when the neurons and circuits are damaged by diseases of the central nervous system (CNS). Injuries caused by stroke or trauma often cause immune dysfunction by abrogation of the immune-regulating neural pathways, which leads to an increased risk of infections. Here, I review the structures and functions of the neural pathways connecting the brain and the immune system, and the neurogenic mechanisms of immune dysfunction that emerge after CNS injuries. Recent technological advances in manipulating specific neural circuits have added mechanistic aspects of neuro-immune interactions and their dysfunctions. Understanding the neural bases of immune control and their pathological processes will deepen our knowledge of homeostasis and lead to the development of strategies to cure immune deficiencies observed in various CNS disorders.
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Fletcher, Kylie, Amin Nassar, Alexander M. Menzies, et al. "Safety and efficacy of immune checkpoint inhibitors (ICI) in patients (pts) with pre-existing neurologic autoimmune diseases (NAID) and Parkinson's disease." Journal of Clinical Oncology 42, no. 16_suppl (2024): 2653. http://dx.doi.org/10.1200/jco.2024.42.16_suppl.2653.
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2653 Background: Patients with pre-existing NAID often flare with ICIs; neurological (neuro) immune related adverse events (irAEs) are often morbid or fatal, and little is known about safety of ICI in pts with NAID and other neuro conditions (e.g. Parkinson’s). Thus, we aimed to determine their safety and efficacy in these contexts. Methods: We retrospectively analyzed 71 pts from 5 institutions receiving ICIs with NAIDs and Parkinson’s disease. NAIDs included multiple sclerosis (MS), myasthenia gravis (MG), inflammatory neuropathy, transverse myelitis, Lambert-Eaton, myotonic dystrophy, and multifocal motor neuropathy. We collected demographics, cancer outcomes, NAID characteristics, and safety outcomes. We used descriptive statistics to analyze treatment outcomes, NAID flares, and irAEs. Results: We collected 71 pts, 40 with NAID and 31 with Parkinson’s. 24 had melanoma, 12 non-small cell lung cancer (NSCLC), 3 small cell lung cancer (SCLC), 6 urothelial/bladder, 4 renal cell carcinoma, and 22 other; 60 had metastatic and 11 had localized disease. Median age at ICI start was 72 years (61% male, 39% female); 8 received combination ICI and 63 received monotherapy. Of 40 pts with NAID, 30% had either NAID flares or neurologic irAEs and 33% experienced other (non-neuro) irAEs (Table). Toxicities were particularly severe in MG; 70% (n=7) had MG flare/neuro irAE, 3 of which were fatal. In addition, 31 had Parkinson’s; of these, 12.9% (n=4) had Parkinson’s flares, 3% (n=1) had neuro-irAEs, and 42% (n=13) had other irAEs. One pt died of grade 5 myocarditis/myositis following combination ICI (Table). 5 MS patients responded to therapy (23%), but none were those with NAID flare/neuro irAE. Both MG patients who had non-neuro irAEs responded to treatment. Conclusions: In this cohort of ICI treated pts with prior neuro disorders, we demonstrated that MG pts have high rates of MG flare/neuro irAEs, hospitalizations, and fatalities, but low response rates. In contrast, other NAID (particularly MS) as well as Parkinson’s appeared to have modest risks of flares/neuro irAEs. Notably, Parkinson’s pts had high rates of non-neuro irAEs and response rates. [Table: see text]
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Rossi, Elena, Luciano Mutti, Andrea Morrione, and Antonio Giordano. "Neuro–Immune Interactions in Severe COVID-19 Infection." Pathogens 11, no. 11 (2022): 1256. http://dx.doi.org/10.3390/pathogens11111256.
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SARS-CoV-2 is a new coronavirus that has affected the world since 2019. Interstitial pneumonia is the most common clinical presentation, but additional symptoms have been reported, including neurological manifestations. Severe forms of infection, especially in elderly patients, present as an excessive inflammatory response called “cytokine storm”, which can lead to acute respiratory distress syndrome (ARDS), multiorgan failure and death. Little is known about the relationship between symptoms and clinical outcomes or the characteristics of virus–host interactions. The aim of this narrative review is to highlight possible links between neurological involvement and respiratory damage mediated by pathological inflammatory pathways in SARS-CoV-2 infection. We will focus on neuro–immune interactions and age-related immunity decline and discuss some pathological mechanisms that contribute to negative outcomes in COVID-19 patients. Furthermore, we will describe available therapeutic strategies and their effects on COVID-19 neurological symptoms.
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Stakenborg, Nathalie, and Guy E. Boeckxstaens. "Shining light on the neuro-immune axis in the gut." Immunity 54, no. 5 (2021): 850–52. http://dx.doi.org/10.1016/j.immuni.2021.04.016.
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Korneva, E. A. "Pathways of neuro-immune communication: past and present time, clinical application." Medical Immunology (Russia) 22, no. 3 (2020): 405–18. http://dx.doi.org/10.15789/1563-0625-pon-1974.
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Fundamental studies in neuroimmunophysiology are the keystone for development of new therapeutic approaches to the treatment of infectious, allergic, oncologic and autoimmune diseases. The achievements in this field allowed approving new treatment methods based on irritation of afferent and efferent fibers of autonomic nerves. That became possible due to numerous studies of pathways between the immune and nervous systems performed over last two decades. The milestones in the history of neuroimmune communication research are represented here. The immune system organs – bone marrow, thymus and spleen are coupled to central nervous system (CNS) via sympathetic nerves. Information about LPS and bacteria emergence in peritoneum, intestine and parenchymal organs reaches the brain via parasympathetic pathways. After vagotomy, the brain neurons do not respond to this kind of antigens. The pattern of brain responses to different applied antigens (the EEG changes and the quantity of c-Fos-positive neurons) is specific for definite antigen, like as algorithms of electroneurogram after exposure to different cytokines. Activation of parasympathetic nerves causes the inhibition of inflammation. The entry of any antigens into the body initiates production of cytokines (IL-1, TNFα, IL-6, IFNγ etc.), via specific receptors which are present on peripheral neurons and terminals of vagus nerve, i.e. the vagal afferent terminals and neurons respond to cytokine action, and these signals are transmitted to CNS neurons. The afferent vagal fibers end on the dorsal vagal complex neurons in the caudal part of medulla oblongata. The information about bacterial antigens, LPS and inflammation is transmitted to the brain via afferent autonomic neural pathways. The speed of this process is high and significantly depends on the rates of cytokine production that are transmitters of signals upon the antigen exposure. It is important to emphasize that this events occur within minutes, and the response to the received information proceeds by reflex mechanisms, i.e., within fraction of a second, as exemplified by inflammation (“inflammation reflex”). This is a fundamentally new and revolutionary discovery in the functional studies of immune system regulation. Clinical efficiency of n. vagus stimulation by pulsed ultrasound was shown, being used for the treatment of inflammatory, allergic and autoimmune diseases, e.g., multiple sclerosis, rheumatoid arthritis, renal inflammatory diseases. Electrical stimulation of the vagus nerve reduces the death of animals in septic shock by 80%. The mentioned data have made a revolution in understanding the functional arrangement of immune system in the body. A hypothesis is represented, which suggests how the information on the antigen exposure is transmitted to the brain.
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Managlia, Elizabeth, Deborah Carroll, Andrew Zloza, and Lena Al-Harthi. "Immune Modulation of HIV Replication: Relevance to HIV Immuno- and Neuro-Pathogenesis." Current HIV Research 2, no. 4 (2004): 395–401. http://dx.doi.org/10.2174/1570162043351020.
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Wang, Tian-Qi, Li-Ming Sun, Le-Xin Hao, Yuan Guo, Yue Zhang, and Xin Feng. "Visualized Analysis of Research Hotspots in Acupuncture-Neuro Immunoregulation Based on Bibliometrics." Acupuncture & Electro-Therapeutics Research 46, no. 4 (2021): 259–70. http://dx.doi.org/10.3727/036012921x16281724938078.
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Objective: To review the development of acupuncture and moxibustion-neural network regulation research systematically and comprehensively in China. Method: This study adopted co-word analysis, cluster analysis and other bibliometric methods such as SATI3.2, Citespace and Gephi to visually demonstrate the annual publication volume, cooperation between institutions and co-authorship in the field of acupuncture-neuro immunoregulation research based on the data of more than 70 papers on related topics covering a period of 24 years from 1997 to 2020 in China. Results: The results show that there are three major research institutions in the field of acupuncture-neuro immunoregulation, namely Shanghai, Zhejiang major research institutions in the field of acupuncture-neuro immunoregulation, namely Shanghai, Zhejiang and Heilongjiang Universities of Traditional Chinese Medicine, as well as 7 clusters, including immune function, acupuncture therapy and endogenous opioid peptide. In the future research, a more comprehensive system will be constructed based on the gradually clear relationship between meridians and nerve regulation, humoral regulation, and immune regulation. Application practice will combine traditional acupuncture with modern medicine to create a variety of new therapies, such as electroacupuncture, electric acupuncture, and acupoint injection. Conclusion: The research focus will be expanded on how to improve the clinical efficacy of multiple combined therapies such as acupuncture for the prevention and treatment of diseases through the regulation of immune cells and immune molecules as well as the regulation of the "acupuncture-meridian- neuroendocrine-immune" network.
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Markelov, Vladimir, and Maxim Trushin. "Sympathetic nervous system and neurotransmitters: their possible role in neuroimmunomodulation of multiple sclerosis and some other autoimmune diseases." Open Medicine 1, no. 4 (2006): 313–29. http://dx.doi.org/10.2478/s11536-006-0031-x.
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AbstractMultiple sclerosis is still a disease without a cure. Although intensive research efforts have led to the development of drugs that modify the activity of the disease, most of them have various side effects and are expensive. At the same time it is becoming apparent that some remedies usually used to treat somatic and psychic disorders also have immunomodulating properties, and may help manage multiple sclerosis and other autoimmune diseases. We describe here the role of the sympathetic nervous system in the neuro-immune interaction in multiple sclerosis and other immune diseases with increased cellular immunity as well as neurochemical disturbances that take place in these disorders.
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Murdaca, Giuseppe, Francesca Paladin, Marco Casciaro, Carmelo Mario Vicario, Sebastiano Gangemi, and Gabriella Martino. "Neuro-Inflammaging and Psychopatological Distress." Biomedicines 10, no. 9 (2022): 2133. http://dx.doi.org/10.3390/biomedicines10092133.
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Inflammaging is a low degree of chronic and systemic tissue inflammation associated with aging, and is intimately linked to pro-inflammatory mediators. These substances are involved in the pathogenesis of chronic inflammatory diseases and related psychopathological symptoms. When inflammation and aging affect the brain, we use the term neuro-inflammaging. In this review, we focused on the neuro-inflammatory process typical of advanced ages and the related psychopathological symptoms, with particular attention to understanding the immune-pathogenetic mechanisms involved and the potential use of immunomodulatory drugs in the control of clinical psychological signs. Inflammation and CNS were demonstrated being intimately linked in the neuro-inflammatory loop. IL-1, IL-6, TNF-a, COX and PGE are only partially responsible. BBB permeability and the consequent oxidative stress resulting from tissue damage make the rest. Some authors elaborated the “theory of cytokine-induced depression”. Inflammation has a crucial role in the onset symptoms of psychopathological diseases as it is capable of altering the metabolism of biogenic monoamines involved in their pathogenesis. In recent years, NSAIDs as an adjunct therapy in the treatment of relevant psychopathological disorders associated with chronic inflammatory conditions demonstrated their efficacy. Additionally, novel molecules have been studied, such as adalimumab, infliximab, and etanercept showing antidepressant and anxiolytic promising results. However, we are only at the beginning of a new era characterized by the use of biological drugs for the treatment of inflammatory and autoimmune diseases, and this paper aims to stimulate future studies in such a direction.
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Kytikova, Oxana, Tatyana Novgorodtseva, Marina Antonyuk, Yulia Denisenko, and Tatyana Gvozdenko. "Molecular Targets of Fatty Acid Ethanolamides in Asthma." Medicina 55, no. 4 (2019): 87. http://dx.doi.org/10.3390/medicina55040087.
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Asthma is a common allergic pathology of the respiratory tract that requires the study of mechanisms underlying it, due to severe forms of the disease, which are refractory to therapy. The review is devoted to the search for molecular targets of fatty acid ethanolamides in asthma, in particular palmitoylethanolamide (PEA), which has been successfully used in the treatment of chronic inflammatory and neurodegenerative diseases, in the pathogenesis of which the nervous and immune systems are involved. Recently, the potentially important role of neuro-immune interactions in the development of allergic reactions has been established. Many of the clinical symptoms accompanying allergic airway inflammation are the result of the activation of neurons in the airways, so the attention of researchers is currently focused on neuro-immune interactions, which can play an important role in asthma pathophysiology. A growing number of scientific works confirm that the key molecule in the implementation of these inter-systemic interactions is nerve growth factor (NGF). In addition to its classic role in nervous system physiology, NGF is considered as an important factor associated with the pathogenesis of allergic diseases, particularly asthma, by regulating of mast cell differentiation. In this regard, NGF can be one of the targets of PEA in asthma therapy. PEA has a biological effect on the nervous system, and affects the activation and the degranulation of mast cells.
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Zusinaite, Eva, Aleksandr Ianevski, Diana Niukkanen, et al. "A Systems Approach to Study Immuno- and Neuro-Modulatory Properties of Antiviral Agents." Viruses 10, no. 8 (2018): 423. http://dx.doi.org/10.3390/v10080423.
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There are dozens of approved, investigational and experimental antiviral agents. Many of these agents cause serious side effects, which can only be revealed after drug administration. Identification of the side effects prior to drug administration is challenging. Here we describe an ex vivo approach for studying immuno- and neuro-modulatory properties of antiviral agents, which may be associated with potential side effects of these therapeutics. The current approach combines drug toxicity/efficacy tests and transcriptomics, which is followed by mRNA, cytokine and metabolite profiling. We demonstrated the utility of this approach with several examples of antiviral agents. We also showed that the approach can utilize different immune stimuli and cell types. It can also include other omics techniques, such as genomics and epigenomics, to allow identification of individual markers associated with adverse reactions to antivirals with immuno- and neuro-modulatory properties.
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Nhieu, Jennifer, Yu-Lung Lin, and Li-Na Wei. "CRABP1 in Non-Canonical Activities of Retinoic Acid in Health and Diseases." Nutrients 14, no. 7 (2022): 1528. http://dx.doi.org/10.3390/nu14071528.
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In this review, we discuss the emerging role of Cellular Retinoic Acid Binding Protein 1 (CRABP1) as a mediator of non-canonical activities of retinoic acid (RA) and relevance to human diseases. We first discuss the role of CRABP1 in regulating MAPK activities and its implication in stem cell proliferation, cancers, adipocyte health, and neuro-immune regulation. We then discuss an additional role of CRABP1 in regulating CaMKII activities, and its implication in heart and motor neuron diseases. Through molecular and genetic studies of Crabp1 knockout (CKO) mouse and culture models, it is established that CRABP1 forms complexes with specific signaling molecules to function as RA-regulated signalsomes in a cell context-dependent manner. Gene expression data and CRABP1 gene single nucleotide polymorphisms (SNPs) of human cancer, neurodegeneration, and immune disease patients implicate the potential association of abnormality in CRABP1 with human diseases. Finally, therapeutic strategies for managing certain human diseases by targeting CRABP1 are discussed.
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Nockher, W. A., and H. Renz. "The role of neurotrophins in the pathogenesis of asthma and related diseases: allergy and asthma as prototypic neuro-immune diseases?" Clinical & Experimental Allergy 32, no. 9 (2002): 1266–68. http://dx.doi.org/10.1046/j.1365-2745.2002.01489.x.
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Jiang, Yunqiu, Sunny S. Po, Faris Amil, and Tarun W. Dasari. "Non-invasive Low-level Tragus Stimulation in Cardiovascular Diseases." Arrhythmia & Electrophysiology Review 9, no. 1 (2020): 40–46. http://dx.doi.org/10.15420/aer.2020.01.
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Low-level tragus stimulation (LLTS) is a non-invasive approach of transcutaneous vagus nerve stimulation. LLTS has applications in diseases of multiple systems, including epilepsy, depression, headache and potentially several cardiovascular diseases. LLTS has shown promising results in suppressing AF, alleviating post-MI ventricular arrhythmias and ischaemia-reperfusion injury along with improving diastolic parameters in heart failure with preserved left ventricular ejection fraction (HFpEF). Preliminary pilot clinical studies in patients with paroxysmal AF, HFpEF, heart failure with reduced ejection fraction and acute MI have demonstrated promising results. The beneficial effects are likely secondary to favourable alteration of the sympathovagal imbalance. On-going exploratory work focused on underlying mechanisms of LLTS in cardiovascular disease states and larger scale clinical trials will shed more light on the non-invasive modulation of the neuro-immune axis.
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Tamberi, Lorenza, Alessia Belloni, Armanda Pugnaloni, et al. "The Influence of Myeloid-Derived Suppressor Cell Expansion in Neuroinflammation and Neurodegenerative Diseases." Cells 13, no. 7 (2024): 643. http://dx.doi.org/10.3390/cells13070643.
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The neuro-immune axis has a crucial function both during physiological and pathological conditions. Among the immune cells, myeloid-derived suppressor cells (MDSCs) exert a pivotal role in regulating the immune response in many pathological conditions, influencing neuroinflammation and neurodegenerative disease progression. In chronic neuroinflammation, MDSCs could lead to exacerbation of the inflammatory state and eventually participate in the impairment of cognitive functions. To have a complete overview of the role of MDSCs in neurodegenerative diseases, research on PubMed for articles using a combination of terms made with Boolean operators was performed. According to the search strategy, 80 papers were retrieved. Among these, 44 papers met the eligibility criteria. The two subtypes of MDSCs, monocytic and polymorphonuclear MDSCs, behave differently in these diseases. The initial MDSC proliferation is fundamental for attenuating inflammation in Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS), but not in amyotrophic lateral sclerosis (ALS), where MDSC expansion leads to exacerbation of the disease. Moreover, the accumulation of MDSC subtypes in distinct organs changes during the disease. The proliferation of MDSC subtypes occurs at different disease stages and can influence the progression of each neurodegenerative disorder differently.
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Van Gerven, L., G. Boeckxstaens, and P. Hellings. "Up-date on neuro-immune mechanisms involved in allergic and non-allergic rhinitis." Rhinology journal 50, no. 3 (2012): 227–35. http://dx.doi.org/10.4193/rhino.11.152.
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Non-allergic rhinitis (NAR) is a common disorder, which can be defined as chronic nasal inflammation, independent of systemic IgE-mediated mechanisms. Symptoms of NAR patients mimic those of allergic rhinitis (AR) patients. However, AR patients can easily be diagnosed with skin prick test or allergen-specific IgE measurements in the serum, whereas NAR patients form a heterogeneous group and are difficult to diagnose because of an extensive list of different phenotypes, all varying in severity, underlying etiology and type of inflammation. Characterization of those phenotypes, mechanisms and management of NAR represents one of the major unmet needs in the field of allergic and non-allergic diseases. This review aims at providing a comprehensive overview of the state of the art in classifying the NAR patients and focuses on the neuro-immune mechanisms involved in allergic and non-allergic rhinitis, including reflections on the pathophysiology and the currently available treatment options.
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Говш, E. Govsh, Кирюхина, et al. "Some Immunoendocrine Criteria Protracted Forms of Hysterical Disorders." Journal of New Medical Technologies 21, no. 4 (2014): 67–71. http://dx.doi.org/10.12737/7271.
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The purpose of this study was to identify prognostically unfavorable immune and endocrine development criteria hysterical disorders. The study involved patients with hysterical personality development, hysterical neurosis and healthy donors. Immunological reactions were performed by standard methods, hormonal - immune enzyme analysis. Changes in cellular and humoral immunity in the form of a reduction in the absolute number of T- and B-lymphocytes, decrease the metabolic activity of neutrophils, the ratio of circulating immune complexes of different molecular weight, and lower cortisol levels indicate the involvement of the immune endocrine reactions in the pathogenetic mechanisms of the development of the protracted forms of conversion disorders, and confirm the need for surveys of the immune and hormonal status of patients suffering from hysterical personality development. Identified by the authors the changes in neuro-immune-endocrine system can be regarded as a prognostically unfavorable in the development of hysterical disorders, and involve the use of immunomodulators in the treatment of these diseases.
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Slama Schwok, Anny, and Julien Henri. "Long Neuro-COVID-19: Current Mechanistic Views and Therapeutic Perspectives." Biomolecules 14, no. 9 (2024): 1081. http://dx.doi.org/10.3390/biom14091081.
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Long-lasting COVID-19 (long COVID) diseases constitute a real life-changing burden for many patients around the globe and, overall, can be considered societal and economic issues. They include a variety of symptoms, such as fatigue, loss of smell (anosmia), and neurological–cognitive sequelae, such as memory loss, anxiety, brain fog, acute encephalitis, and stroke, collectively called long neuro-COVID-19 (long neuro-COVID). They also include cardiopulmonary sequelae, such as myocardial infarction, pulmonary damage, fibrosis, gastrointestinal dysregulation, renal failure, and vascular endothelial dysregulation, and the onset of new diabetes, with each symptom usually being treated individually. The main unmet challenge is to understand the mechanisms of the pathophysiologic sequelae, in particular the neurological symptoms. This mini-review presents the main mechanistic hypotheses considered to explain the multiple long neuro-COVID symptoms, namely immune dysregulation and prolonged inflammation, persistent viral reservoirs, vascular and endothelial dysfunction, and the disruption of the neurotransmitter signaling along various paths. We suggest that the nucleoprotein N of SARS-CoV-2 constitutes a “hub” between the virus and the host inflammation, immunity, and neurotransmission.
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Zouali, Moncef. "B Cells at the Cross-Roads of Autoimmune Diseases and Auto-Inflammatory Syndromes." Cells 11, no. 24 (2022): 4025. http://dx.doi.org/10.3390/cells11244025.
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Whereas autoimmune diseases are mediated primarily by T and B cells, auto-inflammatory syndromes (AIFS) involve natural killer cells, macrophages, mast cells, dendritic cells, different granulocyte subsets and complement components. In contrast to autoimmune diseases, the immune response of patients with AIFS is not associated with a breakdown of immune tolerance to self-antigens. Focusing on B lymphocyte subsets, this article offers a fresh perspective on the multiple cross-talks between both branches of innate and adaptive immunity in mounting coordinated signals that lead to AIFS. By virtue of their potential to play a role in adaptive immunity and to exert innate-like functions, B cells can be involved in both promoting inflammation and mitigating auto-inflammation in disorders that include mevalonate kinase deficiency syndrome, Kawasaki syndrome, inflammatory bone disorders, Schnitzler syndrome, Neuro-Behçet’s disease, and neuromyelitis optica spectrum disorder. Since there is a significant overlap between the pathogenic trajectories that culminate in autoimmune diseases, or AIFS, a more detailed understanding of their respective roles in the development of inflammation could lead to designing novel therapeutic avenues.
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Stimmer, Lev, Claire-Maëlle Fovet, and Ché Serguera. "Experimental Models of Autoimmune Demyelinating Diseases in Nonhuman Primates." Veterinary Pathology 55, no. 1 (2017): 27–41. http://dx.doi.org/10.1177/0300985817712794.
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Human idiopathic inflammatory demyelinating diseases (IIDD) are a heterogeneous group of autoimmune inflammatory and demyelinating disorders of the central nervous system (CNS). These include multiple sclerosis (MS), the most common chronic IIDD, but also rarer disorders such as acute disseminated encephalomyelitis (ADEM) and neuromyelitis optica (NMO). Great efforts have been made to understand the pathophysiology of MS, leading to the development of a few effective treatments. Nonetheless, IIDD still require a better understanding of the causes and underlying mechanisms to implement more effective therapies and diagnostic methods. Experimental autoimmune encephalomyelitis (EAE) is a commonly used animal model to study the pathophysiology of IIDD. EAE is principally induced through immunization with myelin antigens combined with immune-activating adjuvants. Nonhuman primates (NHP), the phylogenetically closest relatives of humans, challenged by similar microorganisms as other primates may recapitulate comparable immune responses to that of humans. In this review, the authors describe EAE models in 3 NHP species: rhesus macaques ( Macaca mulatta), cynomolgus macaques ( Macaca fascicularis), and common marmosets ( Callithrix jacchus), evaluating their respective contribution to the understanding of human IIDD. EAE in NHP is a heterogeneous disease, including acute monophasic and chronic polyphasic forms. This diversity makes it a versatile model to use in translational research. This clinical variability also creates an opportunity to explore multiple facets of immune-mediated mechanisms of neuro-inflammation and demyelination as well as intrinsic protective mechanisms. Here, the authors review current insights into the pathogenesis and immunopathological mechanisms implicated in the development of EAE in NHP.
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Pandey, Manoj Kumar. "Exploring Pro-Inflammatory Immunological Mediators: Unraveling the Mechanisms of Neuroinflammation in Lysosomal Storage Diseases." Biomedicines 11, no. 4 (2023): 1067. http://dx.doi.org/10.3390/biomedicines11041067.
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Lysosomal storage diseases are a group of rare and ultra-rare genetic disorders caused by defects in specific genes that result in the accumulation of toxic substances in the lysosome. This excess accumulation of such cellular materials stimulates the activation of immune and neurological cells, leading to neuroinflammation and neurodegeneration in the central and peripheral nervous systems. Examples of lysosomal storage diseases include Gaucher, Fabry, Tay–Sachs, Sandhoff, and Wolman diseases. These diseases are characterized by the accumulation of various substrates, such as glucosylceramide, globotriaosylceramide, ganglioside GM2, sphingomyelin, ceramide, and triglycerides, in the affected cells. The resulting pro-inflammatory environment leads to the generation of pro-inflammatory cytokines, chemokines, growth factors, and several components of complement cascades, which contribute to the progressive neurodegeneration seen in these diseases. In this study, we provide an overview of the genetic defects associated with lysosomal storage diseases and their impact on the induction of neuro-immune inflammation. By understanding the underlying mechanisms behind these diseases, we aim to provide new insights into potential biomarkers and therapeutic targets for monitoring and managing the severity of these diseases. In conclusion, lysosomal storage diseases present a complex challenge for patients and clinicians, but this study offers a comprehensive overview of the impact of these diseases on the central and peripheral nervous systems and provides a foundation for further research into potential treatments.
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Tudorancea, Ivona Maria, Mitică Ciorpac, Gabriela Dumitrița Stanciu, et al. "The Therapeutic Potential of the Endocannabinoid System in Age-Related Diseases." Biomedicines 10, no. 10 (2022): 2492. http://dx.doi.org/10.3390/biomedicines10102492.
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The endocannabinoid system (ECS) dynamically regulates many aspects of mammalian physiology. ECS has gained substantial interest since growing evidence suggests that it also plays a major role in several pathophysiological conditions due to its ability to modulate various underlying mechanisms. Furthermore, cannabinoids, as components of the cannabinoid system (CS), have proven beneficial effects such as anti-inflammatory, immunomodulatory, neuromodulatory, antioxidative, and cardioprotective effects. In this comprehensive review, we aimed to describe the complex interaction between CS and most common age-related diseases such as neuro-degenerative, oncological, skeletal, and cardiovascular disorders, together with the potential of various cannabinoids to ameliorate the progression of these disorders. Since chronic inflammation is postulated as the pillar of all the above-mentioned medical conditions, we also discuss in this paper the potential of CS to ameliorate aging-associated immune system dysregulation.
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Lénárt, Nikolett, David Brough, and Ádám Dénes. "Inflammasomes link vascular disease with neuroinflammation and brain disorders." Journal of Cerebral Blood Flow & Metabolism 36, no. 10 (2016): 1668–85. http://dx.doi.org/10.1177/0271678x16662043.
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The role of inflammation in neurological disorders is increasingly recognised. Inflammatory processes are associated with the aetiology and clinical progression of migraine, psychiatric conditions, epilepsy, cerebrovascular diseases, dementia and neurodegeneration, such as seen in Alzheimer’s or Parkinson’s disease. Both central and systemic inflammatory actions have been linked with the development of brain diseases, suggesting that complex neuro-immune interactions could contribute to pathological changes in the brain across multiple temporal and spatial scales. However, the mechanisms through which inflammation impacts on neurological disease are improperly defined. To develop effective therapeutic approaches, it is imperative to understand how detrimental inflammatory processes could be blocked selectively, or controlled for prolonged periods, without compromising essential immune defence mechanisms. Increasing evidence indicates that common risk factors for brain disorders, such as atherosclerosis, diabetes, hypertension, obesity or infection involve the activation of NLRP3, NLRP1, NLRC4 or AIM2 inflammasomes, which are also associated with various neurological diseases. This review focuses on the mechanisms whereby inflammasomes, which integrate diverse inflammatory signals in response to pathogen-driven stimuli, tissue injury or metabolic alterations in multiple cell types and different organs of the body, could functionally link vascular- and neurological diseases and hence represent a promising therapeutic target.
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Laurindo, Lucas Fornari, Otávio Augusto Garcia Simili, Adriano Cressoni Araújo, et al. "Melatonin from Plants: Going Beyond Traditional Central Nervous System Targeting—A Comprehensive Review of Its Unusual Health Benefits." Biology 14, no. 2 (2025): 143. https://doi.org/10.3390/biology14020143.
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Melatonin is indispensable for the homeostasis of plants and animals. In humans, it can help prevent or be an adjuvant treatment for several diseases mainly related to the immune system, inflammation, and oxidative stress. Moreover, a melatonin-rich diet is linked to several health benefits, such as regulation of circadian rhythm, regulation of the immunological system, epilepsy control, delaying the aging process, and diminishing hormones related to cancer. This review aimed to show the effects of melatonin in diseases beyond its traditional use. The results showed it can present scavenging of free radicals, reducing inflammatory cytokines, and modulating the immune system. Moreover, it can improve insulin resistance, blood pressure, LDL-c, adipose tissue mass, adhesion molecules, endothelial impairment, and plaque formation. These effects result in neuro- and cardioprotection, improvement of liver diseases, rheumatoid arthritis, dermatitis, COVID-19, polycystic ovaries, and sepsis. We conclude that plant melatonin can benefit patients with many diseases besides sleep problems and neurodegeneration. Plant melatonin may be more cost-effective and present fewer adverse events than synthetic. However, more clinical trials should be performed to show adequate doses, formulation, and treatment time.
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Fan, Min, Subash C. B. Gopinath, and Hongjuan Gao. "Gold structured nanourchin as anesthetic biosensor for determining neuroprotective effect." Materials Express 14, no. 4 (2024): 545–50. http://dx.doi.org/10.1166/mex.2024.2640.
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Research has proven that confusion, delirium, and cognitive dysfunction are the common symptoms caused by anesthesia. In general, neuroproteins fluctuation is common during the process of anesthetic treatment. Among others, tau protein was found to the higher fluctuations after the anesthetic process, and it is highly associated with various neuro-related diseases. Monitoring the level of tau protein helps to identify the neuro-related problems during and after the anesthetic processes. This research was focused on developing a tau electrochemical impedance biosensor on aptamer and antibody-modified electrodes. Aptamer and antibody were immobilized on the gold nanourchin with a chemical linker. Gold nanourchin enhances the probe of aptamer and antibody attachment on the electrode and improves the tau protein detection as low as 1 fM [y = 1.5604x − 1.5643; R2 = 0.9681], determined on a linear range from 1 fM to 1 nM. Further, control performances with complementary aptamer and non-immune antibodies fail to change the response of the current, indicating the specific detection of tau protein. This tau sensor detects the tau protein in its lower level and helps to identify the neuro-related problem caused by anesthetics.
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Li, Xi, Guanghua Xiong, Manni Luo, et al. "Peptidoglycan recognition protein PGRP-5 is involved in immune defence and neuro-behavioral disorders in zebrafish embryos." PLOS ONE 20, no. 1 (2025): e0315714. https://doi.org/10.1371/journal.pone.0315714.
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Peptidoglycan recognition proteins (PGRPs) are the evolutionarily highly conserved class of pattern recognition receptors, however, their functions on the innate immune system and neuro-inflammatory response in aquatic organism are still poorly understood. In this study, we systematically investigated the molecular functions of PGRPs in zebrafish embryos. Firstly, we identified three PGRPs in zebrafish and phylogenetic analysis suggested that DrPGRP-5 was a novel member of the PGRP superfamily in evolution. Secondly, the endogenous mRNA levels of DrPGRP-5 were highly expressed in brain and muscle while significantly down-regulated in liver and egg at 72 hpf in zebrafish embryos. Thirdly, the mRNA levels of DrPGRP-5 were greatly elevated after 6 h of E. coli infection but reached its highest value at 24 h after M. luteus stimulation. Moreover, knock-down DrPGRP-5 could significantly reduce the pro-inflammatory cytokines such as TNF-α, IL-1β and IL-6, but increased the expression of anti-inflammatory cytokine TGF-β. On the other hand, the locomotor behavior abilities and the antioxidant enzyme activities such as CAT and SOD were obviously decreased under the DrPGRP-5 KD conditions. Finally, incubation of zebrafish embryos with anti-inflammatory and neuroprotective agents (10 μM Minocycline) can partially rescue the DrPGRP5-regulated locomotor behavior. Taken together, our data suggested that zebrafish PGRP-5 is involved in the innate immune defenses and regulated the neurobehavior and neuro-inflammation, which may provide new strategies for the treatment of neuro-inflammatory diseases in the aquatic organisms.
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CHEN, JIANXIN, ZHENHUA JIA, XIANGCHUN WU, et al. "SELECTING BIOMARKERS FOR PRIMARY HYPERLIPIDEMIA AND UNSTABLE ANGINA IN THE CONTEXT OF NEURO-ENDOCRINE-IMMUNE NETWORK BY FEATURE SELECTION METHODS." Journal of Biological Systems 18, no. 03 (2010): 605–19. http://dx.doi.org/10.1142/s0218339010003433.
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Hyperlipidemia (HL) and unstable angina (UA) are two sequential diseases that cause more and more morbidity and mortality world-wide. Biomarkers selection in the level of physical and chemical specifications (PCS) plays a key role in understanding the pathology of both diseases. Neuro-Endocrine-Immune (NEI) system is a preferable pathway to investigate the interaction network of related PCS in the context of HL and UA. Data mining approaches are a kind of advanced statistical methods to unravel the "secret" of interaction network of PCS in both diseases. Feature selection methods are a branch of data mining approaches to select informative subset of PCS as biomarkers to distinguish a disease from healthy control cohort with high classification accuracy. In this paper, we firstly use three feature selection methods combined with decision tree classification algorithm to select several biomarkers from NEI network. The results show that SVM based decision tree is best fit to select biomarkers for both diseases. Furthermore, we use the theory from Traditional Chinese Medicine (TCM) to divide HL and UA patients into two subgroups. Based on this, we propose a novel feature selection method to distinguish the two subgroups. We combine variance analysis with classification method to select three to four biomarkers for two subgroups in the context of HL and UA respectively, which means that NEI specifications behave differently between two subgroups. According to basic theory of TCM, variant subgroups defined by TCM need to be treated differently. It means that patients with the same disease may be treated in a personalized way. The research efforts in the paper not only to provide a better avenue to understand the nature of diseases, but also to pave a basis to treat two diseases in a personalized way.
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Gupta, Rakesh Kumar, Poonam Wasnik, Deepankar Mondal, and Dhananjay Shukla. "Critical role of keratinocytes in cutaneous immune responses." Exploration of Immunology 4, no. 4 (2024): 502–22. http://dx.doi.org/10.37349/ei.2024.00155.
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Keratinocytes play an integral role in the human epidermis, serving as a barrier between the internal and external environment. They are immune-competent cells involved in both innate and adaptive cutaneous immune responses, crucial for maintaining skin integrity. Keratinocytes are essential for epidermal repair, facilitating proliferation and re-epithelialization following injury. They secrete pro-inflammatory markers such as cytokines and chemokines, which promote the recruitment of inflammatory cells like polymorphs and macrophages to the site of skin injury. The immune response mediated by keratinocytes involves signaling molecules like tumor necrosis factor (TNF), interleukin (IL)-1β, and IL-6. Langerhans cells respond to factors secreted by keratinocytes, migrating towards draining lymph nodes to activate T cells and initiate an adaptive immune response. Additionally, keratinocytes express Toll-like receptors (TLRs), enabling them to detect molecular patterns of pathogens. Recent studies have focused on understanding these interactions of keratinocytes to develop therapeutic strategies for managing various skin diseases. Genetic defects in keratinocytes underlie conditions like psoriasis. We also discuss the role of keratinocytes and the effect of neuro-endocrinal signaling and interventions, associated corticosteroidogenic pathways, and response to UV radiations to maintain a state of homeostasis. This article underlines and improves our understanding of the immune function of keratinocytes, which is crucial for developing more effective therapies against skin diseases.
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Tauber, M., and L. Basso. "Neuro-immune interactions in allergic skin diseases." Revue Française d'Allergologie, June 2021. http://dx.doi.org/10.1016/j.reval.2021.05.001.
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Wu, Wanhua, Jianing Li, Su Chen, and Suidong Ouyang. "The airway neuro-immune axis as a therapeutic target in allergic airway diseases." Respiratory Research 25, no. 1 (2024). http://dx.doi.org/10.1186/s12931-024-02702-8.
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AbstractRecent evidence has increasingly underscored the importance of the neuro-immune axis in mediating allergic airway diseases, such as allergic asthma and allergic rhinitis. The intimate spatial relationship between neurons and immune cells suggests that their interactions play a pivotal role in regulating allergic airway inflammation. Upon direct activation by allergens, neurons and immune cells engage in interactions, during which neurotransmitters and neuropeptides released by neurons modulate immune cell activity. Meanwhile, immune cells release inflammatory mediators such as histamine and cytokines, stimulating neurons and amplifying neuropeptide production, thereby exacerbating allergic inflammation. The dynamic interplay between the nervous and immune systems suggests that targeting the neuro-immune axis in the airway could represent a novel approach to treating allergic airway diseases. This review summarized recent evidence on the nervous system’s regulatory mechanisms in immune responses and identified potential therapeutic targets along the peripheral nerve-immune axis for allergic asthma and allergic rhinitis. The findings will provide novel perspectives on the management of allergic airway diseases in the future.
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Straub, Rainer H., and Maurizio Cutolo. "A history of psycho-neuro-endocrine immune interactions in rheumatic diseases." Neuroimmunomodulation, August 21, 2024. http://dx.doi.org/10.1159/000540959.
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Background All active scientists stand on the shoulders of giants and many other more anonymous scientists, and this is not different in our field of psycho-neuro-endocrine immunology in rheumatic diseases. Too often, the modern world of publishing forgets about the collective enterprise of scientists. Some journals advise the authors to present only literature of the last decade, and it became a natural attitude of many scientists to present only the latest publications. In order to work against this general unempirical behavior, Neuroimmunomodulation devotes the 30-year anniversary issue to the history of medical science in psycho-neuro-endocrine immunology. Summary Keywords were derived from the psycho-neuro-endocrine immunology research field very well known to the authors (R.H.S. collects a list of key words since 1994). We screened PubMed, the Cochran Library of Medicine, Embase, Scopus database, and the ORCiD database to find relevant historical literature. The Snowballing procedure helped to find related work. According to the historical appearance of discoveries in the field, the order of presentation follows the subsequent scheme: 1. The sensory nervous system, 2. The sympathetic nervous system, 3. The vagus nerve, 4. Steroid hormones (glucocorticoids, androgens, progesterone, estrogens, and the vitamin D hormone), 5. Afferent pathways involved in fatigue, anxiety, insomnia, and depression (in-cludes pathophysiology), and 6. Evolutionary medicine and energy regulation – an umbrella theory. Key Messages A brief history on psycho-neuro-endocrine immunology cannot address all relevant aspects of the field. The authors are aware of this shortcoming. The reader must see this review as a viewpoint through the biased eyes of the authors. Nevertheless, the text gives an overview of history in psycho-neuro-endocrine immunology of rheumatic diseases.
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Zhu, Yan, Shixin Duan, Mei Wang, Zhili Deng, and Ji Li. "Neuroimmune Interaction: A Widespread Mutual Regulation and the Weapons for Barrier Organs." Frontiers in Cell and Developmental Biology 10 (May 11, 2022). http://dx.doi.org/10.3389/fcell.2022.906755.
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Since the embryo, the nervous system and immune system have been interacting to regulate each other’s development and working together to resist harmful stimuli. However, oversensitive neural response and uncontrolled immune attack are major causes of various diseases, especially in barrier organs, while neural-immune interaction makes it worse. As the first defense line, the barrier organs give a guarantee to maintain homeostasis in external environment. And the dense nerve innervation and abundant immune cell population in barrier organs facilitate the neuroimmune interaction, which is the physiological basis of multiple neuroimmune-related diseases. Neuroimmune-related diseases often have complex mechanisms and require a combination of drugs, posing challenges in finding etiology and treatment. Therefore, it is of great significance to illustrate the specific mechanism and exact way of neuro-immune interaction. In this review, we first described the mutual regulation of the two principal systems and then focused on neuro-immune interaction in the barrier organs, including intestinal tract, lungs and skin, to clarify the mechanisms and provide ideas for clinical etiology exploration and treatment.
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Sudeep Kumar Brahma. "NEURO-ENDOCRINE-IMMUNE MODULATION BY AYURVEDIC RASAYANA DRUGS." International Journal of Ayurveda and Pharma Research, January 13, 2021, 51–71. http://dx.doi.org/10.47070/ijapr.v8i12.1734.
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Ayurveda which literally means “the science of life” is the ancient Indian system of medicine. Rasayana is a specialized branch of Ayurveda. The drugs attributed with Rasayana properties are mentioned to delay the process of ageing, enhance the mental and cognitive functions and deliver freedom from a number of diseases including those caused by infectious organisms. All these activities of Rasayana drugs seem to be associated with neuro-endocrine-immune systems. In this study we have reviewed the growing inter-relationship between the neuro-endocrine-immune systems and stress as a neuro-endocrine-immune phenomenon. Some important Ayurvedic Rasayana drugs including Aswagandha (Withania somnifera), Tulsi (Ocimum sanctum), Guduchi (Tinospora cordifolia), Shilajit (Asphalt), Brahmi (Bacopa monnieri) and few others along with their pharmacological actions on the above three systems and stress as well have also been reviewed. It has been observed that most of them tend to exhibit their activities by modulating the neuro-endocrine-immune systems along with anti-stress/adaptogenic capability. The scientific inter-relationship between the three systems has been taken as the model reference. Similar actions are expected from other Rasayana drugs too. Therefore Rasayana drugs in Ayurveda can be evaluated and used as neuro-endocrine-immune modulators.
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De Luca, Ciro, Anna Maria Colangelo, Lilia Alberghina, and Michele Papa. "Neuro-Immune Hemostasis: Homeostasis and Diseases in the Central Nervous System." Frontiers in Cellular Neuroscience 12 (November 26, 2018). http://dx.doi.org/10.3389/fncel.2018.00459.
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Hou, Xiaoxiao, and David Artis. "Neuro-immune cell interactions in the regulation of intestinal immune homeostasis." Current Opinion in Gastroenterology, October 18, 2024. http://dx.doi.org/10.1097/mog.0000000000001065.
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Purpose of the review Bidirectional regulation between neurons and immune cells in the intestine governs essential physiological processes, including digestion, metabolism and motility, while also controlling intestinal inflammation and maintaining tissue homeostasis. This review covers recent advances and future research challenges focused on the regulatory molecules and potential therapeutic targets in neuron-immune interactions within the intestine. Recent findings Recently identified molecular and cellular pathways have been shown to regulate neuron-immune cell cross talk in the context of maintaining tissue homeostasis, modulating inflammation, and promoting intestinal repair. Additionally, behaviors governed by the central nervous system, including feeding and stress responses, can play key roles in regulating intestinal immunity and inflammation. Summary This review emphasizes recent progress in understanding the complex interplay between the nervous system and intestinal immune system and outlines future research directions. These advances have the potential to lead to innovative therapies targeting gastrointestinal disorders including inflammatory bowel diseases, allergic responses and cancer.
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Lepennetier, Gildas, Zsuzsanna Hracsko, Marina Unger, et al. "Cytokine and immune cell profiling in the cerebrospinal fluid of patients with neuro-inflammatory diseases." Journal of Neuroinflammation 16, no. 1 (2019). http://dx.doi.org/10.1186/s12974-019-1601-6.
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Abstract Background Cytokines play multiple roles during neuro-inflammatory processes and several cytokines have been studied in the context of specific diseases. This study provides a comprehensive picture of cerebrospinal fluid (CSF) changes during neuro-inflammation by analyzing multiple cytokines in combination with immune cell subsets and standard CSF parameters. Methods Using multiplex assays, we simultaneously measured 36 cytokines (CCL1–3, CCL7, CCL8, CCL11, CCL13, CCL19, CCL20, CCL22–27, CXCL1, CXCL2, CXCL5, CXCL6, CXCL8, CXCL9, CXCL11–13, CXCL16, CX3CL1, IL2, IL4, IL6, IL10, IL16, GM-CSF, IFNγ, MIF, TNFα, and MIB1β) in the CSF and serum of 75 subjects. Diagnoses included clinically isolated syndrome and relapsing-remitting multiple sclerosis (MS, n = 18), secondary progressive MS (n = 8), neuro-syphilis (n = 6), Lyme neuro-borreliosis (n = 13), bacterial and viral meningitis (n = 20), and patients with non-inflammatory neurological diseases (NIND, n = 10). Cytokine concentrations were correlated with CSF standard parameters and CSF immune cell subsets (CD4 and CD8 T cells, B cells, plasmablasts, monocytes, and NK cells) quantified by flow cytometry. Results We observed increased levels of multiple cytokines (26/36) in patients with neuro-inflammatory diseases when compared to NIND that consistently correlated with CSF cell count and QAlbumin. Most CSF cytokine concentrations correlated with each other, but correlations between CSF and serum values were scarce (3/36). Within the CSF compartment, CXCL13 showed a strong association with B cells when analyzing all patients, as well as patients with an intact blood-brain barrier (BBB). NK cells positively correlated with CSF concentrations of multiple cytokines (22/36) when analyzing all patients. These correlations were maintained when looking at patients with a disrupted BBB but not detectable in patients with an intact BBB. Conclusions Under conditions of neuro-inflammation, multiple CSF cytokines are regulated in parallel and most likely produced locally. A combined increase of CSF CXCL13 levels and B cells occurs under conditions of an intact BBB. Under conditions of a disrupted BBB, CSF NK cells show significantly increased values and seem to have a major contribution to overall inflammatory processes, reflected by a strong correlation with multiple cytokines. Future studies are necessary to address the exact kinetics of these cytokines during neuro-inflammation and their relation to specific diseases phenotypes.
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You, Xin-yu, Han-yu Zhang, Xu Han, Fang Wang, Peng-wei Zhuang, and Yan-jun Zhang. "Intestinal Mucosal Barrier Is Regulated by Intestinal Tract Neuro-Immune Interplay." Frontiers in Pharmacology 12 (May 31, 2021). http://dx.doi.org/10.3389/fphar.2021.659716.
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Inflammatory bowel disease, irritable bowel syndrome and severe central nervous system injury can lead to intestinal mucosal barrier damage, which can cause endotoxin/enterobacteria translocation to induce infection and is closely related to the progression of metabolic diseases, cardiovascular and cerebrovascular diseases, tumors and other diseases. Hence, repairing the intestinal barrier represents a potential therapeutic target for many diseases. Enteral afferent nerves, efferent nerves and the intrinsic enteric nervous system (ENS) play key roles in regulating intestinal physiological homeostasis and coping with acute stress. Furthermore, innervation actively regulates immunity and induces inherent and adaptive immune responses through complex processes, such as secreting neurotransmitters or hormones and regulating their corresponding receptors. In addition, intestinal microorganisms and their metabolites play a regulatory role in the intestinal mucosal barrier. This paper primarily discusses the interactions between norepinephrine and β-adrenergic receptors, cholinergic anti-inflammatory pathways, nociceptive receptors, complex ENS networks, gut microbes and various immune cells with their secreted cytokines to summarize the key roles in regulating intestinal inflammation and improving mucosal barrier function.