牛多形核白细胞(PMN)中P38 MAPK,PKC和PI3-K介导的NADPH氧化酶激活和吞噬作用(英文)

P38 MAPK, PKC and PI3-K Mediate NADPH Oxidase Activation and Phagocytosis in Bovine PMN

用血清调理的酵母聚糖（ｓｅｒｕｍ－ｏｐｓｏｎｉｚｅｄ ｚｙｍｏｓａｎ ，ｓＯＺ）刺激多性核白细胞（ＰＭＮ）引起的Ｏ２－产生受到ｐ３８ＭＡＰＫ抑制物（ＳＢ２０３５８０），ＰＩ３－Ｋ抑制物（ｗｏｒｔｍａｎｎｉｎ）和ＰＫＣ抑制物（ＧＦ１０９２０３Ｘ）的明显抑制，这些抑制物也明显引起ｓＯＺ诱导的一种ＮＡＤＰＨ氧化酶的胞浆成分 ｐ４７ｐｈｏｘ的磷酸化。可是流式细胞分析表明，ＳＢ２０３５８０和 ｗｏｒｔｍａｎｎｉｎ使吞噬作用减弱，而 ＧＦＩＯ９２０３Ｘ使吞噬作用增强。这些结果表明，虽然ＰＩ３－Ｋ和ｐ３８ ＭＡＰＫ都参与ＮＡＤＰＨ氧化酶激活和吞噬作用的信号传导，但ＮＡＤＰＨ氧化酶激活的信号传导途径与吞噬作用的信号传导途径不同。

O2-production by bovine polymorphonuclear leukocytes(PMN) stimulated with serumopsonized zymosan(sOZ) was significantly inhibited by an inhibitor of p38 MAPK(SB203580), an inhibitor of PI3-K(wortmannin) and an inhibitor of PKC(GF109203X) .These inhibitors also caused significant attenuation of sOZ-induced phosphorylation of p47phox, a cytosolic component of NADPH oxidase. However, flow cyto- metric analysis revealed that while SB203580 and wortmannin attenuated phagocytosis, GF109203x faciloitated it...