Paper Information

Journal:   GOVARESH JOURNAL   FALL 2015 , Volume 20 , Number SUPPLEMENT; Page(s) 32 To 32.
 
Paper: 

AUTONOMIC NERVOUS SYSTEM AND COLITIS

 
 
Author(s):  MAGHOOL FATEMEH*, EMAMI MOHAMMAD HASSAN
 
* DEPARTMENT OF PHYSIOLOGY, SCHOOL OF MEDICINE, ISFAHAN UNIVERSITY OF MEDICAL SCIENCES, ISFAHAN, IRAN
 
Abstract: 

Introduction: Inflammatory bowel diseases (IBD), including ulcerative colitis (UC) and crohn’s disease(CD), are characterized by a chronic relapsing remitting course as a result of intestinal inflammation. Increased intestinal epithelial barrier (IEB) permeability during chronic inflammation is a key factor in IBD pathogenesis. The preservation of gastrointestinal (GI) mucosal integrity depends on the rapid alarm of protective mechanisms in the face of pending injury. Two main inflammatory control mechanisms are included: the innate immune responses and brain derived immunoregulatory output. More recent evidences reveal that the parasympathetic nervous system (PNS) comprised by the vagus nerve (VN) is a major player in neuroimmune cross-talk which exerts potent immunomodulatory effects on inflammatory responses. It subserves this goal through the different mechanisms. Autonomic dysfunctions has been reported earlier in IBD patients. In this context, the role of the cholinergic system in the regulation of the gut immune responses has fuelled an increased interest in recent years. In this review, we will discuss the current mechanisms involved in the cholinergic anti-inflammatory pathway in the GI tract and describe how the alterations of the cholinergic system activity participate in the development of IBD.
Methods: Integrative literature review was performed in the following databases: MEDLINE/ PubMed, SciVerse Scopus, and ISI Web of Science.
Key search terms were “crohn’s disease”; “autonomic nervous system”; “inflammation”; and “ulcerative colitis.32 articles were selected for this review.
Results: The selected literature show that Ach protects epithelial cells from the detrimental effects of proinflammatory cytokines on the integrity of the IEB via activation of its muscarinic receptors (mAchR).
It also suppresses the splenic immune cell activation and alters interaction between dendritic cells (DCs) and T cells in experimental colitis.
Conclusion: Deeper investigation on the molecular mechanisms underlying this counter-regulatory neuroimmune mechanism will open new therapeutic avenues for the treatment of IBD.

 
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