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

ABSTRACT:

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% O₂ 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% 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-? and IL-6 were suppressed in IL-3^-/- mice compared with WT mice. Moreover, the hyperoxia-induced the activation of I?B? kinase (IKK) ?, I?B? phosphorylation, and nuclear factor-?B 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.

SUBMITTER: Huang Z 

PROVIDER: S-EPMC6206653 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature