Toll-Like Receptor mRNA Expression Is Selectively Increased in the Colonic Mucosa of Two Animal Models Relevant to Irritable Bowel Syndrome
TLR3
Intestinal mucosa
DOI:
10.1371/journal.pone.0008226
Publication Date:
2009-12-09T00:05:30Z
AUTHORS (7)
ABSTRACT
Irritable bowel syndrome (IBS) is largely viewed as a stress-related disorder caused by aberrant brain-gut-immune communication and altered gastrointestinal (GI) homeostasis. Accumulating evidence demonstrates that stress modulates innate immune responses; however, very little known on the immunological effects of GI tract. Toll-like receptors (TLRs) are critical pattern recognition molecules system. Activation TLRs bacterial viral leads to activation NF-kB an increase in inflammatory cytokine expression. It was our hypothesis receptor expression may be changed tract animals with stress-induced IBS-like symptoms.In this study, objective evaluate TLR profile colonic mucosa two rat strains display visceral hypersensitivity; stress-sensitive Wistar-Kyoto (WKY) maternally separated (MS) rat. Quantitative PCR TLR2-10 mRNA both proximal distal mucosae carried out adulthood. Significant increases seen levels TLR3, 4 & 5 MS rats compared controls. No significant differences were noted for 2, 7, 9 10 while 6 could not detected any samples strains. The WKY strain have increased 4, 5, 8, control Sprague-Dawley strain. found TLR2 before TLR6 all strains.These data suggest early life genetic predisposition affect key sentinels system which direct relevance molecular pathophysiology IBS.
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