Abstract
BackgroundInterleukin (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.MethodsHyperoxic ALI was induced in wild-type (WT) and IL-3 gene disrupted (IL-3−/−) mice by exposure to 100% O2 for 72 h.ResultsHyperoxia 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% O2 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.ConclusionsOur results suggest IL-3 is a potential therapeutic target for hyperoxia-induced ALI.
Highlights
Effects of IL-3 on lung injury and mortality in hyperoxiainduced acute lung injury (ALI) Hyperoxia caused significant neutrophil infiltration, alveolar capillary protein leak, and lung edema after 72 h, which could be dampened in IL-3−/− mice (Fig. 1b, c, d, and e)
When IL-3−/− mice were treated with hyperoxia, the lung histological changes were reduced compared with WT mice (Fig.1f; Fig. 2)
A total of 50% of the mice in the WT mice treated hyperoxia group died within 24 h, and an additional 50% died within 72 h, while 60% of the mice in the IL-3−/− mice treated hyperoxia group survived
Summary
Acute lung injury (ALI) is a mild form of ARDS. Inflammation is thought to contribute to the pathogenesis of ALI/ARDS [1,2,3,4,5], as ALI/ARDS is characterized by increased vascular permeability, extravasation of plasma, and neutrophil infiltration in the lung [1,2,3,4]. It is bewildering that the results from clinical trials of novel anti-inflammatory strategies for ALI/ARDS have been disappointingly negative [1, 2, 4, 7]. These results reflect an incomplete understanding of ALI/ARDS pathogenesis.
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