Interleukin-28B dampens protease-induced lung inflammation via IL-25 and TSLP inhibition in epithelial cells

Inflammation via Epithelial-Derived IL-25 Viral-Induced Th2-Type Allergic NK Cell Deficiency Predisposes to

Protease Allergens Induce the Expression of IL-25 via Erk and p38 MAPK Pathway

Allergic diseases, including asthma, are characterized by T helper type 2 (Th2) cell-mediated inflammations, coupled with tissue infiltration by eosinophils. In this study, we demonstrate that multiple protease allergens, including papain and DerP1, efficiently induce interleukin (IL)-25 and thymic stromal lymphopoietin (TSLP) gene expression, and this phenomenon is dependent on the protease ac...

Soluble uric acid induces inflammation via TLR4/NLRP3 pathway in intestinal epithelial cells

Objective(s): Hyperuricemia is a risk for cardiovascular and metabolic diseases, but the mechanism is ambiguous. Increased intestinal permeability is correlated with metabolic syndrome risk factors. Intestinal epithelial cells play a pivotal role in maintaining intestinal permeability. Uric acid is directly eliminated into intestinal lumen, however, the mechanism and e...

Hyperoxia increases interleukin-17 in airway epithelial cells, alveolar type II cells and alveolar macrophages after ovalbumin-induced lung inflammation

Methods The experimental design was approved by the Ethics Committee of Federal University of Ouro Preto (UFOP)No.092/2012. Groups of female BALB/c mice (8 weeks old; 24.53±0.31g) were divided randomly in to five experimental groups as follows: Control group (CG) remained to air room; PBS group received aluminum hydroxide in phosphate buffered saline (PBS); OVA group (OVA) received ovalbumin an...

The critical role of epithelial-derived Act1 in IL-17- and IL-25-mediated pulmonary inflammation.

IL-25 initiates, promotes, and augments Th2 immune responses. In this study, we report that Act1, a key component in IL-17-mediated signaling, is an essential signaling molecule for IL-25 signaling. Although Act1-deficient mice showed reduced expression of KC (CXCL1) and neutrophil recruitment to the airway compared with wild-type mice in response to IL-17 stimulation, Act1 deficiency abolished...