Interleukin-3 plays a vital role in hyperoxic acute lung injury in mice via mediating inflammation

Interleukin (IL)-3 amplifies inflammation. However, the effect of IL-3 in acute lung injury (ALI), an acute inflammatory disease, is unclear. The aim of this study was to test the hypothesis that IL-3 plays an important role in hyperoxia-induced ALI. Hyperoxic ALI was induced in wild-type (WT) and IL-3 gene disrupted (IL-3 −/− ) mice by exposure to 100% O 2 for 72 h. Hyperoxia increased IL-3 levels in plasma and lung tissues in WT mice. Pulmonary inflammation and edema were detected by histological assay in WT mice exposed to 100% O 2 for 72 h. However, the hyperoxia-induced lung histological changes were improved in IL-3 −/− mice. The hyperoxia-induced elevation of neutrophils in bronchoalveolar lavage fluids and circulation were reduced in IL-3 −/− mice. Meanwhile, the levels of tumor necrosis factor-α and IL-6 were suppressed in IL-3 −/− mice compared with WT mice. Moreover, the hyperoxia-induced the activation of IκBα kinase (IKK) β, IκBα phosphorylation, and nuclear factor-κB translocation were inhibited in IL-3 −/− mice compared with WT mice. Our results suggest IL-3 is a potential therapeutic target for hyperoxia-induced ALI.