Tissue- and Stimulus-Dependent Role of Phosphatidylinositol 3-Kinase Isoforms for Neutrophil Recruitment Induced by Chemoattractants In Vivo

摘要: PI3K plays a fundamental role in regulating neutrophil recruitment into sites of inflammation but the different isoforms remains unclear. In this study, we evaluated PI3Kγ and PI3Kδ for influx induced by exogenous administration or endogenous generation chemokine CXCL1. Administration CXCL1 −/− wild-type (WT) mice similar increases leukocyte rolling, adhesion, emigration cremaster muscle when examined intravital microscopy. The induction pleural cavity tibia-femoral joint injection was not significantly WT mice. Neutrophil altered treatment with specific inhibitor, IC87114, AS605240. IC87114 prevented CXCL1-induced only presence inhibitor Ag challenge immunized CXCR2-dependent that inhibited wortmannin blockade to bronchoalveolar lavage exogenously added production accumulation neutrophils lung tissues treated IC87114. C5a fMLP appeared rely solely on PI3Kγ. Altogether, our data demonstrate there is tissue- stimulus-dependent chemoattractants vivo.