| First Author | Bhandari V | Year | 2007 |
| Journal | J Immunol | Volume | 178 |
| Issue | 8 | Pages | 4993-5000 |
| PubMed ID | 17404281 | Mgi Jnum | J:145286 |
| Mgi Id | MGI:3834073 | Doi | 10.4049/jimmunol.178.8.4993 |
| Citation | Bhandari V, et al. (2007) Increased hyperoxia-induced mortality and acute lung injury in IL-13 null mice. J Immunol 178(8):4993-5000 |
| abstractText | IL-13 is a critical effector at sites of Th2 inflammation and remodeling. As a result, anti-IL-13-based therapies are being actively developed to treat a variety of diseases and disorders. However, the beneficial effects of endogenous IL-13 in the normal and diseased lung have not been adequately defined. We hypothesized that endogenous IL-13 is an important regulator of oxidant-induced lung injury and inflammation. To test this hypothesis, we compared the effects of 100% O(2) in mice with wild-type and null IL-13 loci. In this study, we demonstrate that hyperoxia significantly augments the expression of the components of the IL-13R, IL-13Ralpha1, and IL-4Ralpha. We also demonstrate that, in the absence of IL-13, hyperoxia-induced tissue inflammation is decreased. In contrast, in the IL-13 null mice, DNA injury, cell death, caspase expression, and activation and mortality are augmented. Interestingly, the levels of the cytoprotective cytokines vascular endothelial cell growth factor, IL-6, and IL-11 were decreased in the bronchoalveolar lavage fluid. These studies demonstrate that the expression of the IL-13R is augmented and that the endogenous IL-13-IL-13R pathway contributes to the induction of inflammation and the inhibition of injury in hyperoxic acute lung injury. |
