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首页> 外文期刊>American Journal of Physiology >Role of phosphatidylinositol 3-kinase-gamma in mediating lung neutrophil sequestration and vascular injury induced by E. coli sepsis.
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Role of phosphatidylinositol 3-kinase-gamma in mediating lung neutrophil sequestration and vascular injury induced by E. coli sepsis.

机译：磷脂酰肌醇3-激酶-γ在介导肺中性粒细胞螯合和大肠杆菌败血症诱导的血管损伤中的作用。

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摘要

We addressed the in vivo role of phosphatidylinositol 3-kinase-gamma (PI3K-gamma) in signaling the sequestration of polymorphonuclear leukocytes (PMNs) in lungs and in the mechanism of inflammatory lung vascular injury. We studied mice with deletion of the p110 catalytic subunit of PI3K-gamma (PI3K-gamma(-/-) mice). We measured lung tissue PMN sequestration, microvascular permeability, and edema formation after bacteremia induced by intraperitoneal Escherichia coli challenge. PMN infiltration into the lung interstitium in PI3K-gamma(-/-) mice as assessed morphometrically was increased 100% over that in control mice within 1 h after bacterial challenge. PI3K-gamma(-/-) mice also developed a greater increase in lung microvascular permeability after E. coli challenge, resulting in edema formation. The augmented lung tissue PMN sequestration in PI3K-gamma(-/-) mice was associated with increased expression of the PMN adhesive proteins CD47 and beta(3)-integrins. We observed increased association of CD47 andbeta(3)-integrins with the extracellular matrix protein vitronectin in lungs of PI3K-gamma(-/-) mice after E. coli challenge. PMNs from these mice also showed increased beta(3)-integrin expression and augmented beta(3)-integrin-dependent PMN adhesion to vitronectin. These results point to a key role of PMN PI3K-gamma in negatively regulating CD47 and beta(3)-integrin expression in gram-negative sepsis. PI3K-gamma activation in PMNs induced by E. coli may modulate the extent of lung tissue PMN sequestration secondary to CD47 and beta(3)-integrin expression. Therefore, the level of PI3K-gamma activation may be an important determinant of PMN-dependent lung vascular injury.
机译：我们解决了磷脂酰肌醇3-激酶-γ（PI3K-γ）在体内信号化肺中多形核白细胞（PMN）的隔离和炎症性肺血管损伤的机制中的体内作用。我们研究了缺失PI3K-γp110催化亚基的小鼠（PI3K-γ（-/-）小鼠）。我们测量了腹膜内大肠杆菌激发引起的菌血症后的肺组织PMN隔离，微血管通透性和水肿形成。经形态学评估，PM3渗入PI3K-γ（-/-）小鼠的肺间质比对照小鼠在细菌攻击后1小时内增加了100％。 PI3K-gamma（-/-）小鼠在大肠杆菌攻击后还产生了更大的肺微血管通透性增加，导致水肿形成。增强的肺组织PMN隔离在PI3K-γ（-/-）小鼠中与PMN粘附蛋白CD47和beta（3）-整合素的表达增加有关。我们观察到的大肠杆菌攻击后，PI3K-γ（-/-）小鼠的肺中CD47和beta（3）-整合素与细胞外基质蛋白玻连蛋白的关联增加。这些小鼠的PMN还显示出增加的beta（3）-整合素表达和增加的beta（3）-整合素依赖性PMN对玻连蛋白的粘附。这些结果表明，PMNPI3K-γ在革兰氏阴性脓毒症中负调节CD47和beta（3）-整合素表达中起关键作用。由大肠杆菌诱导的PMN中的PI3K-γ激活可能会调节继发于CD47和β（3）-整合素表达的肺组织PMN隔离的程度。因此，PI3K-γ激活水平可能是PMN依赖性肺血管损伤的重要决定因素。

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