研究嗜中性白细胞呼吸爆发的信号转导中磷脂酰肌醇3位激酶信号通路的作用，特别是它与涞氖芴澹璆蛋白- 磷脂酶C - 肌醇三磷酸通路的关系，以及该通路在防止细胞凋亡和调控细胞骨架肌动蛋白聚合上所起的作用。该信号通路的研究不仅对提高人体免疫功能和治疗有关疾病有重要意义，而且有助于了解其它细胞中磷脂酰肌醇3位激酶信号通路的作用。

The neutrophils constitute the largest population of white cells and the first line of defense of mammalian organisms against invading microbes. A variety of deseases are caused by disfunction of the neutrophils. .In this investigation, the effects of the monoclonal antibody directed against type II phosphatidylinositol 4-kinase (PI4K) and other inhibitor on theN-formyl- methionyl-leucyl-phenylalanine (fMLP)-stimulated respiratory burst in neutrophils were studied. It was found that the antibody inhibited the fMLP-stimulated respiratory burst. However, even at higher concentration, the antibody could not completely.inhibit the cell response. The maximal inhibition of the fMLP-stimulated respiratory burst by the antibody against type II PI4K was found to be about 70%, whereas the PI4K activity was inhibited by only about 40%. The discrepancy in depressing the cell response and the enzyme activity may be the result of depletion of the phosphatidylinositol 4,5-bisphosphate pools during the incubation of cells with the antibody. Both the 40% inhibition of PI4K activity and 70% depression of the respiratory burst by the type II PI4K antibody may imply that at least 40% of the phosphatidylinositol 4,5-biphosphate was synthesized promptly by all forms of PI4K and phosphatidylinositol-4-phosphate 5-kinase in the fMLP-activated cells. The results suggest that PI4K plays a central role in either phospholipase C or PI3K signaling and that PI3K, PI4K, and phosphatidylinositol 4-phosphate 5-kinase must be considered as an integrated family for the phosphatidylinositol 3,4,5-trisphosphate initiated signaling..To define the role of phospholipase C (PLC) and phosphatidylinositol 3-kinase (PI3K) signaling pathways in arachidonic acid (AA) stimulated respiratory burst in human neutrophils, the AA dose-dependent respiratory burst and PI3K activity, the AA-induced cytoplasmic Ca2+ mobilization, as well as the effects of U73122 and wortmannin on both signaling pathways were investigated. It was found that U73122 effectively inhibited the AA-stimulated respiratory burst and the Ca2+ release from intracellular store but not the PI3K activity, indicating the involvement of PLC signaling and the independence of PI3K signaling on PLC activity. Wortmannin at the concentration, which was sufficient to inhibit PI3K activity, can only partly inhibited the Ca2+ release from internal store in the stimulated cells, indicating the existence of two pathways initiated by different PLC subfamilies: PI3K-regulated and PI3K-independent. The present study suggests that both the PLC signaling pathway, which may be activated by PLCb and PLCg respectively, and the PI3K signaling pathway are involved in the arachidonic acid stimulated respiratory burst in human neutrophil..