作者: Vanessa Pinho , Danielle G Souza , Michele M Barsante , Fabiana P Hamer , Marta S De Freitas
DOI: 10.1189/JLB.0704386
关键词:
摘要: Thephosphatidylinositol-3 kinase (PI3K) family of signaling enzymes plays a crucial role in leukocyte recruitment and activation hence, likely regulates the induction propagation phases inflammation. However, little data have emerged showing for these processes resolution phase models vivo Here, we evaluated PI3K migration survival eosinophils model allergic pleurisy mice. Eosinophil accumulation PI3K-deficient mice was inhibited at 48 h, as compared with wild-type but not earlier time-points (6 24 h). Experiments adop- tive transfer bone marrow showed that non-bone marrow-derived cells required their accumulation. Systemic treatment inhibitors before antigen challenge prevented eosino- phils. This associated decreased Akt phos- phorylation, interleukin-5 production, phil release from marrow. Treatment h after mark- edly cleared accumulated eosinophils, an effect inhibition phosphorylation increased number apoptotic events. Al- together, our demonstrate important maintenance eosinophilic in- flammation vivo, whereas other isoforms may be relevant process. J. Leukoc. Biol. 77: 800-810; 2005.