Bacteria- and host-derived mechanisms to control intestinal epithelial cell homeostasis: implications for chronic inflammation.

Bacteria- and host-derived mechanisms to control intestinal epithelial cell homeostasis: implications for chronic inflammation. Research Abstract Details 

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Bacteria- and host-derived mechanisms to control intestinal epithelial cell homeostasis: implications for chronic inflammation. Abstract Text:

Thomas Clavel,Dirk Haller,Thomas Clavel,Dirk Haller,

The genetic predisposition to deregulated mucosal immune responses and the concurrent prevalence of certain environmental triggers in developed countries are strong etiologic factors for the development of inflammatory bowel diseases in human subjects, including Crohn's disease and ulcerative colitis. Numerous clinical and experimental studies have shown that the intestinal microbes are critical for the initiation and progression of chronic intestinal inflammation. Activation of pattern recognition receptor signaling via members of the Toll-like receptor (TLR) and the nucleotide-binding oligomerization domain (NOD)-like families initiates inflammatory defense mechanisms that are required to alert and protect the host. Key inflammatory mechanisms such as nuclear transcription factor kappaB (NF-kappaB) activation and endoplasmic reticulum stress responses are controlled by a complex network of pathways that includes intrinsic feedback effectors and is targeted by immunosuppressive cytokines such as interleukin 10 (IL-10) and transforming growth factor (TGF)-beta. In the absence or after functional loss of these antiinflammatory feedback signals, physiological defense mechanisms may turn into pathological responses. The data discussed in the present review suggest that disturbances in the homeostasis between bacteria- and host-derived signals at the epithelial cell level lead to a break in the intestinal barrier function and to the development of mucosal immune disorders in genetically susceptible hosts.

Bacteria- and host-derived mechanisms to control intestinal epithelial cell homeostasis: implications for chronic inflammation. Publishing Authors By Initials

T Clavel,D Haller,T Clavel,D Haller,

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Bacteria- and host-derived mechanisms to control intestinal epithelial cell homeostasis: implications for chronic inflammation. Journal Published:

PUBLICATION TYPE: Review

Journal: Inflammatory bowel diseases

VOLUME: 13

Page Numbers: 1153-64

Journal Abbreviation: Inflamm. Bowel Dis.

ISSN: 1078-0998

DAY: 9

MONTH: Sep

YEAR: 2007

Bacteria- and host-derived mechanisms to control intestinal epithelial cell homeostasis: implications for chronic inflammation. Information

Number of References: 155

LANGUAGE: eng

NlmUniqueID: 9508162

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Grant and Affiliation Information for Bacteria- and host-derived mechanisms to control intestinal epithelial cell homeostasis: implications for chronic inflammation.

AFFILIATION: Technical University of Munich, Experimental Nutritional Medicine, Else Kröner-Fresenius-Center, Freising-Weihenstephan, Germany.

Country: United States

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MEDLINETA: Inflamm Bowel Dis

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