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Review
. 2004;29(1-3):55-68.
doi: 10.1385/IR:29:1-3:055.

Intestinal epithelial cell regulation of mucosal inflammation

Affiliations
Review

Intestinal epithelial cell regulation of mucosal inflammation

Yimin Yu et al. Immunol Res. 2004.

Abstract

The intestinal epithelium serves as one of human's primary interfaces with the outside world. This interface is very heavily colonized with bacteria and yet permits absorption of life-sustaining nutrients while protecting the tissues below from microbial onslaught. Although the gut epithelium had been classically thought to achieve this function primarily by functioning as a passive, albeit highly selective, barrier, research over the last decade has demonstrated that in fact the epithelium plays a very active role in protecting the host from the bacteria that colonize it. As a consequence of its mediation of mucosal immunity, intestinal epithelial dysfunction appears to be central to diseases associated with aberrant gut mucosal immune responses such as inflammatory bowel disease (IBD). This article reviews: (1) how the gut epithelium participates in regulating innate immune inflammatory responses to enteric pathogens, (2) how these responses may regulate the adaptive immune system, (3) mechanisms that may resolve acute inflammation, and (4) how epithelial dysfunction may participate in regulating both the active and chronic phases of IBD.

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References

    1. Infect Agents Dis. 1996 Jan;5(1):1-7 - PubMed
    1. Prostaglandins. 1997 Feb;53(2):107-37 - PubMed
    1. Science. 2000 Sep 1;289(5484):1560-3 - PubMed
    1. J Clin Invest. 1997 Jun 1;99(11):2588-601 - PubMed
    1. Science. 1998 Dec 11;282(5396):2085-8 - PubMed

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