Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 426901
Title Epithelial crosstalk at the microbiota-mucosal interface
Author(s) Wells, J.; Rossi, O.; Meijerink, M.; Baarlen, P. van
Source Proceedings of the National Academy of Sciences of the United States of America 108 (2011)Suppl. 1. - ISSN 0027-8424 - p. 4607 - 4614.
DOI http://dx.doi.org/10.1073/pnas.1000092107
Department(s) Host Microbe Interactomics
WIAS
Publication type Refereed Article in a scientific journal
Publication year 2011
Keyword(s) toll-like receptor-4 - intestinal dendritic cells - antigen-presenting cells - growth-factor-beta - factor-kappa-b - immune-response - lamina propria - crohns-disease - paneth cells - stromal cells
Abstract This article provides an overview of how intestinal epithelial cells (IEC) recognize commensals and how they maintain host-bacterial symbiosis. Endocrine, goblet cells, and enterocytes of the intestinal epithelium express a range of pattern recognition receptors (PRR) to sense the presence of microbes. The best characterized are the Toll-like receptors (TLR) and nucleotide oligomerization domain-like receptors (NLR), which play a key role in pathogen recognition and the induction of innate effectors and inflammation. Several adaptations of PRR signaling have evolved in the gut to avoid uncontrolled and potentially destructive inflammatory responses toward the resident microbiota. PRR signaling in IEC serve to maintain the barrier functions of the epithelium, including the production of secretory IgA (sIgA). Additionally, IECs play a cardinal role in setting the immunosuppressive tone of the mucosa to inhibit overreaction against innocuous luminal antigens. This includes regulation of dendritic cells (DC), macrophage and lymphocyte functions by epithelial secreted cytokines. These immune mechanisms depend heavily on IEC recognition of microbes and are consistent with several studies in knockout mice that demonstrate TLR signaling in the epithelium has a profoundly beneficial role in maintaining homeostasis
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