| First Author | Huang Z | Year | 2018 |
| Journal | BMC Pulm Med | Volume | 18 |
| Issue | 1 | Pages | 164 |
| PubMed ID | 30373540 | Mgi Jnum | J:285791 |
| Mgi Id | MGI:6400144 | Doi | 10.1186/s12890-018-0725-2 |
| Citation | Huang Z, et al. (2018) Interleukin-3 plays a vital role in hyperoxic acute lung injury in mice via mediating inflammation. BMC Pulm Med 18(1):164 |
| abstractText | 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-alpha and IL-6 were suppressed in IL-3(-/-) mice compared with WT mice. Moreover, the hyperoxia-induced the activation of IkappaBalpha kinase (IKK) beta, IkappaBalpha phosphorylation, and nuclear factor-kappaB 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. |
