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IL-6 and Stat3 are required for survival of intestinal epithelial cells and development of colitis-associated cancer.
It is demonstrated that IL-6 is a critical tumor promoter during early CAC tumorigenesis and the NF-kappaB-IL-6-Stat3 cascade is an important regulator of the proliferation and survival of tumor-initiating IECs. Expand
IKKβ Links Inflammation and Tumorigenesis in a Mouse Model of Colitis-Associated Cancer
It is shown that although deletion of IKKbeta in intestinal epithelial cells does not decrease inflammation, it leads to a dramatic decrease in tumor incidence without affecting tumor size, which is linked to increased epithelial apoptosis during tumor promotion. Expand
A distinct array of proinflammatory cytokines is expressed in human colon epithelial cells in response to bacterial invasion.
Since the cytokines expressed in response to bacterial invasion or other proinflammatory agonists have a well documented role in chemotaxis and activation of inflammatory cells, colon epithelial cells appear to be programmed to provide a set of signals for the activation of the mucosal inflammatory response in the earliest phases after microbial invasion. Expand
Secretion of proinflammatory cytokines by epithelial cells in response to Chlamydia infection suggests a central role for epithelial cells in chlamydial pathogenesis.
Findings suggest a novel pathophysiologic concept wherein the acute host response to Chlamydia at mucosal surfaces is primarily initiated and sustained by epithelial cells, the first and major targets of chlamydial infection. Expand
Nod2 Mutation in Crohn's Disease Potentiates NF-κB Activity and IL-1ß Processing
Variants of NOD2, an intracellular sensor of bacteria-derived muramyl dipeptide (MDP), increase susceptibility to Crohn's disease (CD). These variants are thought to be defective in activation ofExpand
Paneth cells directly sense gut commensals and maintain homeostasis at the intestinal host-microbial interface
It is established that gut epithelia actively sense enteric bacteria and play an essential role in maintaining host-microbial homeostasis at the mucosal interface and that epithelial MyD88 signaling limited bacterial penetration of host tissues. Expand
Adenoma-linked barrier defects and microbial products drive IL-23/IL-17-mediated tumour growth
It is proposed that barrier deterioration induced by colorectal-cancer-initiating genetic lesions results in adenoma invasion by microbial products that trigger tumour-elicited inflammation, which in turn drives tumour growth. Expand
Maintenance of colonic homeostasis by distinctive apical TLR9 signalling in intestinal epithelial cells
The data provide a case for organ-specific innate immunity in which TLR expression in polarized IECs has uniquely evolved to maintain colonic homeostasis and regulate tolerance and inflammation. Expand
Expression and regulation of the human beta-defensins hBD-1 and hBD-2 in intestinal epithelium.
HBD-1 and hBD-2 may be integral components of epithelial innate immunity in the intestine, with each occupying a distinct functional niche in intestinal mucosal defense. Expand
A NOD2–NALP1 complex mediates caspase-1-dependent IL-1β secretion in response to Bacillus anthracis infection and muramyl dipeptide
NOD2 plays a key role in the B. anthracis-induced inflammatory response by being a critical mediator of IL-1β secretion, and caspase-1 and NOD2 depend on each other for this role. Expand