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23 - Gastrointestinal Inflammation and Ulceration: Mediators of Induction and Resolution

from PART V - INFLAMMATORY DISEASES/HISTOLOGY

Published online by Cambridge University Press:  05 April 2014

Linda Vong
Affiliation:
McMaster University
Paul L. Beck
Affiliation:
University of Calgary Calgary
John L. Wallace
Affiliation:
McMaster University
Charles N. Serhan
Affiliation:
Harvard Medical School
Peter A. Ward
Affiliation:
University of Michigan, Ann Arbor
Derek W. Gilroy
Affiliation:
University College London
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Summary

The gastrointestinal (GI) tract is composed of a series of organs whose collective aim is to extract and absorb nutrients from food, and expel undigested matter as waste. As the lumen of the GI tract is essentially outside of the body, it is not surprising to find that the physical interface between “self” and the outside world is quite complex. The gut must be able to withstand fluctuations associated with changes in temperature, pH, and osmolarity, as well as overcome and respond to microbiota residence and the associated release of immunostimulatory molecules and detergent-like substances. As such, the mucosa has evolved to act as a first line of defense, its repertoire including (1) the spatial secretion of protective substances (acid, bicarbonate, and mucus); (2) the presence of tight junctions to limit the passive diffusion of harmful substances; (3) the mucosal microcirculation which enables rapid dilution/removal of noxious stimuli; and (4) the mucosal immune system where resident and blood-borne immunocytes and granulocytes are mobilized to initiate an appropriate inflammatory response. This so-called mucosal defense is supported by a catalogue of endogenous mediators; together these act to dampen the inflammatory response, which results from the aggressive accumulation of tissue-damaging metabolites.

The aim of this chapter is to review current knowledge regarding mediators involved in the pathogenesis of GI disease, with particular reference to nonsteroidal anti-inflammatory drug (NSAID)-induced gastropathy and colitis. We will address mediators that play a key role in the proresolution phase of inflammation, and discuss some of the new therapeutic approaches aimed at promoting mucosal healing and tissue homeostasis.

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Chapter
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Publisher: Cambridge University Press
Print publication year: 2010

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References

Fiorucci, S., Distrutti, E., Cirino, G., and Wallace, J.L. 2006. The emerging roles of hydrogen sulfide in the gastrointestinal tract and liver. Gastroenterology 131:259–271.CrossRefGoogle ScholarPubMed
Gilroy, D.W., and Perretti, M. 2005. Aspirin and steroids: new mechanistic findings and avenues for drug discovery. Curr Opin Pharmacol 5:405–411.CrossRefGoogle ScholarPubMed
Serhan, C.N. 2007. Resolution phase of inflammation: novel endogenous anti-inflammatory and proresolving lipid mediators and pathways. Annu Rev Immunol 25:101–137.CrossRefGoogle ScholarPubMed
Wallace, J.L., and Del Soldato, P. 2003. The therapeutic potential of NO-NSAIDs. Fundam Clin Pharmacol 17:11–20.CrossRefGoogle ScholarPubMed
Wallace, J.L., and Devchand, P.R. 2005. Emerging roles for cyclooxygenase-2 in gastrointestinal mucosal defence. Br J Pharmacol 145:275–282.CrossRefGoogle Scholar
Xavier, R.J., and Podolsky, D.K. 2007. Unravelling the pathogenesis of inflammatory bowel disease. Nature 448:427–434.CrossRefGoogle ScholarPubMed

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