English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

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.

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