NDLI: Toll-like receptor 3 signaling enables human esophageal epithelial cells to sense endogenous danger signals released by necrotic cells

Content Provider	PubMed Central
Author	Lim, Diana M. Wang, Mei-lun
Copyright Year	2011
Abstract	The mechanisms by which gastroesophageal reflux disease esophagitis develops are controversial. Although many support the notion that caustic injury leads to reflux esophagitis, others have proposed that reflux esophagitis is caused by esophageal epithelial cytokine-mediated inflammation. We previously demonstrated that Toll-like receptor 3 (TLR3) is highly expressed and functional in the nontransformed human esophageal epithelial cell line EPC2-hTERT. In addition to activation by viral double-stranded RNA, TLR3 can be activated by endogenous mRNA released by necrotic cells. In the present study, we investigated the role of esophageal epithelial TLR3 to sense danger signals released by necrotic esophageal epithelial cells in vitro. Following induction of freeze-thaw necrosis, necrotic EPC2-hTERT cell supernatants (NCS) were used to stimulate EPC2-hTERT monolayers, leading to NF-κB-dependent induction of IL-8 mRNA expression. Responses to self-derived NCS were not observed in transformed gastrointestinal epithelial cell lines, including TE-1 and Caco-2 cells, suggesting that the ability to sense endogenous danger signals is unique to nontransformed esophageal epithelial cells. To determine the immunostimulatory role of epithelial RNA, EPC2-hTERT cells were stimulated with self-derived mRNA, which significantly induced IL-8 mRNA expression. Finally, suppression of TLR3 signaling in a DN-TLR3 cell line, hTERT-ΔTIR-TLR3, led to reduced NCS-induced IL-8 induction by both NCS and mRNA stimulation. Our results demonstrate that human esophageal epithelial cells can sense endogenous danger signals, in part through TLR3 signaling. This supports the concept that epithelial injury plays an inciting role in the pathogenesis of reflux-induced esophagitis, providing important insights into the mechanisms by which epithelial injury leads to inflammation.
Related Links	http://dx.doi.org/10.1152/ajpgi.00471.2010
Starting Page	91
File Format	PDF
ISSN	01931857
e-ISSN	15221547
Journal	American Journal of Physiology - Gastrointestinal and Liver Physiology
Issue Number	1
Volume Number	301
Language	English
Publisher	American Physiological Society
Publisher Date	2011-07-01
Access Restriction	Open
Rights Holder	American Physiological Society
Subject Keyword	Hepatology Gastroenterology Physiology (medical) Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Hepatology Physiology Physiology (medical) Gastroenterology

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