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

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: Our results suggest IL-3 is a potential therapeutic target for hyperoxia-induced ALI. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12890-018-0725-2) contains supplementary material, which is available to authorized users.