Th2 cytokine IL-4 is critical in initiating pulmonary vascular inflammation under hypoxic conditions and induces pulmonary vascular endothelial cell activation.

IL-4-mediated pro-inflammatory vascular responses have been implicated in the pathogenesis of chronic cardiopulmonary diseases. Our results show that hypoxia-induced collagen synthesis and early recruitment of inflammatory cells are significantly less in the lungs of IL-4 knockout (KO) mice than in those of wild-type mice. In addition, we found that IL-4 significantly increased pro-inflammatory genes in primary pulmonary microvascular endothelial cells. This study was designed to identify the gene expression profile of IL-4-dependent pulmonary vascular inflammation induced by hypoxia.