| First Author | Aden K | Year | 2016 |
| Journal | Oncogenesis | Volume | 5 |
| Issue | 11 | Pages | e270 |
| PubMed ID | 27869785 | Mgi Jnum | J:264487 |
| Mgi Id | MGI:6120601 | Doi | 10.1038/oncsis.2016.71 |
| Citation | Aden K, et al. (2016) Classic IL-6R signalling is dispensable for intestinal epithelial proliferation and repair. Oncogenesis 5(11):e270 |
| abstractText | Inflammatory bowel disease is characterized by disturbed cytokine signalling in the mucosa. Inhibition of the proinflammatory interleukin (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 contributes 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 to IL-6 classic signalling. Mice deficient in intestinal IL-6R (IL-6R(DeltaIEC) mice) did not display increased susceptibility to acute dextran sulfate sodium (DSS)-induced colitis. In the azoxymethane DSS model IL-6R(DeltaIEC) mice were not protected from inflammation-induced carcinogenesis but showed comparable tumor load to wild-type mice. These data indicate that classic signalling is not the major pathway to transduce IL-6 stimuli into the intestinal epithelium. |
