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https://www.selleckchem.com/products/ly2584702.html 02; 95%CI, 1.01-1.03; P = 0.004). Sensitivity analyses demonstrated consistent results and indicated no directional pleiotropy-e.g., MR-Egger (OR, 1.03; 95%CI, 1.01-1.05; P = 0.002; P intercept =0.37). In the stratified analysis, the significant association persisted across asthma phenotypes-e.g., childhood asthma (OR, 1.05; 95%CI, 1.02-1.08; P less then 0.001) and obese asthma (OR, 1.02; 95%CI 1.01-1.03; P = 0.007). Sensitivity analysis using 16 variants selected with different thresholds also demonstrated significant associations with overall asthma and its phenotypes. Conclusion Genetically-instrumented soluble interleukin-6 receptor level was causally associated with modestly but significantly higher risks of asthma and its phenotypes. Our observations support further investigations into identifying specific endotypes in which interleukin-6 pathways may play major roles.Background Interleukin-22 (IL-22) impacts the integrity of intestinal epithelia and has been associated with the development of colitis-associated cancer and inflammatory bowel diseases (IBD). Previous data suggest that IL-22 protects the mucosal barrier and promotes wound healing and barrier defect. We hypothesized, that IL-22 modulates cell polarity of intestinal epithelial cells (IECs) acting on tight junction assembly. The aim of the study was to investigate IL-22-dependent mechanisms in the reprogramming of intestinal epithelia. Methods IECs were exposed to IL-22 at various concentrations. IECs in Matrigel® were grown to 3-dimensional cysts in the presence or absence of IL-22 and morphology and expression of polarity proteins were analyzed by confocal microscopy. Epithelial cell barrier (TER and sandwich assay) and TJ assembly analysis (calcium-switch assay) were performed. TJ and cell polarity protein expression were assessed by western blotting and confocal microscopy. Cell migration and invasion assayrelevant for cell survival. In additi

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