Classic IL-6R signalling is dispensable for intestinal epithelial proliferation and repair

Title of publication: 

Classic IL-6R signalling is dispensable for intestinal epithelial proliferation and repair

Authors: 

Aden K, Breuer A, Geese H, Tran F, Sommer J, Waetzig G, Reinheimer T, Schreiber S, Rose-John S, Scheller J, Rosenstiel P, Rehman A

Year of Publication: 

2016

medium resp. publishing house / place: 

Oncogenesis

edition / issue: 

Nov 21

Pages: 

5(11):e270.

related to project: 

Inflammatory bowel disease is characterized by disturbed cytokine signalling in the mucosa. The inhibition of the proinflammatory IL-6 pathway is a promising new therapeutic strategy, but safety concerns arise as IL-6 signalling also contributes to epithelial repair of the intestinal mucosa. To which extent IL-6 classic or trans-signalling contribute to intestinal repair remains elusive. We tested the influence of IL-6 classic signalling on intestinal repair and proliferation Whereas IL-6 induced STAT3 phosphorylation in the colonic cancer cell lines, primary non malignant intestinal organoids did not respond IL-6 classic signalling. Mice deficient in intestinal IL-6R (IL-6R∆IEC mice) did not display increased susceptibility to acute DSS induced colitis. In the AOM DSS model IL-6R∆IEC mice were not protected from inflammation-induced carcinogenesis but showed comparable tumor load compared to wildtype mice. These data indicate that classic signalling is not the major pathway to transduces IL-6 stimuli into the intestinal epithelium.