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Protoplasma

, Volume 249, Issue 4, pp 871–886

First Online: 17 November 2011Received: 06 October 2011Accepted: 11 October 2011

Abstract

Inflammatory bowel disease IBD is a chronic disease arising due to a culmination of genetic, environmental, and lifestyle-associated factors and resulting in an excessive pro-inflammatory response to bacterial populations in the gastrointestinal tract. The prevalence of IBD in developing nations is relatively low, and it has been proposed that this is directly correlated with a high incidence of helminth infections in these areas. Gastrointestinal nematodes are the most prevalent parasitic worms, and they efficiently modulate the immune system of their hosts in order to establish chronic infections. Thus, they may be capable of suppressing unrelated inflammation in disorders such as IBD. This review describes how nematodes, or their products, suppress innate and adaptive pro-inflammatory immune responses and how the mechanisms involved in the induction of anti-nematode responses regulate colitis in experimental models and clinical trials with IBD patients. We also discuss how refinement of nematode-derived therapies should ultimately result in the development of potent new therapeutics of clinical inflammatory disorders.

KeywordsInflammatory bowel disease Crohn’s disease Immune modulation Gastrointestinal nematodes Nematode therapy AbbreviationsAAMAlternatively activated macrophage

CDCrohn’s disease

DCDendritic cell

DSSDextran sodium sulfate

DNBSDinitrobenzene sulfonic acid

IBDInflammatory bowel disease

IFNInterferon

ESExcretory-secretory

Foxp3Forkhead box P3

ILInterleukin

mLNMesenteric lymph node

MPOMyeloperoxidase

RELMResistin-like molecule

TGFTransforming growth factor

ThT helper cell

TLRToll-like receptor

TNBSTrinitrobenzenesulfonic acid

TNFTumor necrosis factor

TregRegulatory T cell

TSLPThymic stromal lymphopoietin

UCUlcerative colitis

Handling Editor: David Robinson

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Author: Rose A. K. Whelan - Susanne Hartmann - Sebastian Rausch

Source: https://link.springer.com/







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