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Regulation of Antimicrobial Pathways by Endogenous Heat Shock Proteins in Gastrointestinal Disorders

1
Department of Microbiology & Immunology, Dalhousie University, 5850 College Street, Room 7-C, Halifax, NS B3H 4R2, Canada
2
Division of Pediatric Gastroenterology and Nutrition, Department of Pediatrics, Dalhousie University, IWK Health Centre, 5850/5980 University Avenue, Halifax, NS B3K 6R8, Canada
*
Author to whom correspondence should be addressed.
Gastrointest. Disord. 2019, 1(1), 39-56; https://doi.org/10.3390/gidisord1010005
Received: 31 August 2018 / Revised: 23 September 2018 / Accepted: 26 September 2018 / Published: 28 September 2018
Heat shock proteins (HSPs) are essential mediators of cellular homeostasis by maintaining protein functionality and stability, and activating appropriate immune cells. HSP activity is influenced by a variety of factors including diet, microbial stimuli, environment and host immunity. The overexpression and down-regulation of HSPs is associated with various disease phenotypes, including the inflammatory bowel diseases (IBD) such as Crohn’s disease (CD). While the precise etiology of CD remains unclear, many of the putative triggers also influence HSP activity. The development of different CD phenotypes therefore may be a result of the disease-modifying behavior of the environmentally-regulated HSPs. Understanding the role of bacterial and endogenous HSPs in host homeostasis and disease will help elucidate the complex interplay of factors. Furthermore, discerning the function of HSPs in CD may lead to therapeutic developments that better reflect and respond to the gut environment. View Full-Text
Keywords: heat shock protein; Crohn’s disease; inflammatory bowel disease; NOD2; immune homeostasis heat shock protein; Crohn’s disease; inflammatory bowel disease; NOD2; immune homeostasis
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Finlayson-Trick, E.; Connors, J.; Stadnyk, A.; Van Limbergen, J. Regulation of Antimicrobial Pathways by Endogenous Heat Shock Proteins in Gastrointestinal Disorders. Gastrointest. Disord. 2019, 1, 39-56.

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