Cox-2 Is Regulated by Toll-Like Receptor-4 (TLR4) Signaling: Role in Proliferation and Apoptosis in the Intestine

Abstract

Background-We have recently demonstrated that mice deficient in TLR4 or its adapter molecule MyD88 have increased signs of colitis compared to wild-type (WT) mice following dextran sodium sulfate (DSS)-induced injury. We wished to test the hypothesis that Cox-2 derived PGE 2 is important in TLR4-related mucosal repair.

Enterotoxigenic Bacteroides fragilis: A potential instigator of colitis

“…Administration of DSS to induce subclinical colitis, while convenient, does not yield a model that perfectly mimics the pathogenesis of IBD, since DSS causes a chemical colitis through epithelial injury. 26 Nevertheless, DSS has been commonly used to study the pathogenesis of colitis 18,[26][27][28][29][30][31] and was useful to allow us to model the clinical scenarios of ETBF colonization preceding or following the emergence of colitis in the host. Another potential study limitation was the use of antibiotics to enhance bacterial colonization.…”

Effects of Muclin (Dmbt1) deficiency on the gastrointestinal system

“…DMBT1 has been reported to be regulated by the NOD2-signaling component of the innate defense system, and it is upregulated in inflamed tissue in Crohn's patients (46). Knockout of other innate defense genes has been shown to either increase (17) or decrease (34) the severity of experimental colitis. Because the DMBT1 product gp340 is involved in innate defenses, we explored whether Muclin deficiency would affect DSS-induced colitis.…”

Prostaglandin-secreting cells: a portable first aid kit for tissue repair

“…TLR/MyD88 signaling is responsible for both transcriptional regulation of Ptgs2 (7,20) and increased Ptgs2 protein expression by macrophages (20). In the proximal colon, Ptgs2 seems to play a primary role in negatively regulating the acute infiltration of leukocytes upon DSS-induced injury (13).…”