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首页> 外文期刊>Journal of Cellular Physiology >Acute endotoxemia prolongs the survival of rat lung neutrophils in response to 12-O-tetradecanoyl-phorbol 13-acetate.
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Acute endotoxemia prolongs the survival of rat lung neutrophils in response to 12-O-tetradecanoyl-phorbol 13-acetate.

机译：急性内毒素延长大鼠的生存肺中性粒细胞在回应12-O-tetradecanoyl-phorbol 13-acetate。

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摘要

Acute endotoxemia is associated with prolonged survival of adherent neutrophils in the lung vasculature. In the present studies, the effects of inflammatory mediators on signaling pathways regulating neutrophil survival were examined. We found that the protein kinase C activator, 12-O-tetradecanoyl-phorbol 13-acetate (TPA), but not interferon-gamma (IFN-gamma), prolonged the survival of adherent vasculature lung neutrophils from endotoxemic rats, a response that was correlated with reduced apoptosis. Although endotoxin administration to rats induced the expression of the anti-apoptotic protein Mcl-1 in lung neutrophils, TPA had no effect on this response. Endotoxin administration also induced expression of total p38 and p44/42 mitogen activated protein kinases (MAPK) in neutrophils, as well as phosphatidyl inositol 3 kinase (PI3K) and its downstream target protein kinase B (PKB). Treatment of the cells with TPA increased p38 MAPK expression in cells from both control and endotoxin treated animals. Cells from endotoxin treated, but not control animals, were found to exhibit constitutive binding activity of nuclear factor kappa B (NF-kappaB) which was blocked by TPA. In contrast, constitutive CCAAT/enhancer binding protein (C/EBP) nuclear binding activity evident in neutrophils from control animals was reduced following endotoxin administration. Moreover, this response was independent of TPA. These data suggest that NF-kappaB plays a role in TPA-induced signaling leading to prolonged survival of adherent vascular neutrophils in the lung during acute endotoxemia.
机译：急性内毒素与长期相关联附着在肺中性粒细胞的生存脉管系统。信号通路的炎症介质调节中性粒细胞生存。发现蛋白激酶C的激活,12-O-tetradecanoyl-phorbol 13-acetate (TPA),但是不是移行细胞(IFN-gamma),延长了附着脉管系统肺中性粒细胞的生存endotoxemic老鼠的反应与细胞凋亡减少。老鼠诱导内毒素管理mcl1抗凋亡蛋白的表达肺中性粒细胞,TPA没有影响响应。总p38的表达和p44/42促分裂原在中性粒细胞激活蛋白激酶(MAPK),以及磷脂酰肌醇3激酶(PI3K)及其下游靶蛋白激酶B (PKB)。治疗的细胞与TPA p38增加从控制和MAPK表达细胞内毒素对待动物。治疗,但不是控制动物,被发现展览本构绑定的核活动因子k B (NF-kappaB)被TPA。结合蛋白(C / EBP)核绑定活动在中性粒细胞明显控制动物减少内毒素后管理。此外,这种反应是TPA的独立。这些数据表明,NF-kappaB起着作用TPA-induced信号导致长时间附着血管中中性粒细胞的生存在急性肺内毒素。

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