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-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.

journal_name

BMC Pulm Med

journal_title

BMC pulmonary medicine

authors

Huang Z,Zhang W,Yang J,Sun F,Zhou H

doi

10.1186/s12890-018-0725-2

subject

Has Abstract

pub_date

2018-10-30 00:00:00

pages

164

issue

1

issn

1471-2466

pii

10.1186/s12890-018-0725-2

journal_volume

18

pub_type

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