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Inhibition of phospholipase D blocks activation of fibrinogen-adherent neutrophils by tumor necrosis factor.

机译:磷脂酶D的抑制可阻止肿瘤坏死因子激活纤维蛋白原粘附的中性粒细胞。

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摘要

Tumor necrosis factor stimulates fibrinogen-adherent neutrophils to produce a dramatic oxidative burst; the resulting superoxide and other products may contribute to tissue damage in severe infection. Inhibitors of the phospholipase D pathway blocked this activation without affecting cell adherence or nonspecific activation by phorbol myristate acetate. The phospholipase D pathway appears to be involved in the activation of adherent neutrophils by tumor necrosis factor, and this pathway may be a target for modulation of tumor necrosis factor's effects.
机译:肿瘤坏死因子刺激纤维蛋白原粘附的中性粒细胞产生剧烈的氧化爆发;所产生的超氧化物和其他产物可能会导致严重感染中的组织损伤。磷脂酶D途径的抑制剂在不影响细胞粘附或肉豆蔻酸乙酸佛波酯非特异性激活的情况下阻断了该激活。磷脂酶D途径似乎参与了肿瘤坏死因子对粘附的中性粒细胞的活化,并且该途径可能是调节肿瘤坏死因子作用的靶标。

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