Interleukin-10 counterregulates proinflammatory cytokine-induced inhibition of neutrophil apoptosis during severe sepsis
Interleukin-10 counterregulates proinflammatory cytokine-induced inhibition of neutrophil apoptosis during severe sepsis
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DOI：
10.1182/blood.v90.9.3356
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发表时间：
1997-11-01
期刊：
影响因子：
20.3
通讯作者：
Ertel, W
中科院分区：
文献类型：
--
作者：
Keel, M;Ungethum, U;Ertel, W
中性粒细胞在脓毒性多器官功能障碍综合征（MODS）的病理生理学中起着关键作用，通过过量释放有毒颗粒成分和活性氧代谢产物，从而导致组织破坏。脓毒症期间衰老的中性粒细胞的增加表明自身调节机制的潜在破坏，包括从炎症部位去除活化的中性粒细胞的凋亡过程。因此，本研究探讨严重脓毒症患者中性粒细胞凋亡及其调控机制。与健康个体相比，严重脓毒症患者的自发性中性粒细胞凋亡显著减少。脓毒症期间在循环中检测到的细胞因子（肿瘤坏死因子-α [TNF-α]、干扰素-γ [IFN-γ]、粒细胞集落刺激因子[G-CSF]、粒细胞-巨噬细胞集落刺激因子[GM-CSF]）抑制了两组中的中性粒细胞凋亡，尽管这种作用在健康人的中性粒细胞中更为明显。健康人中性粒细胞加入脂多糖（LPS）后，中性粒细胞的白细胞数明显增加（P
Neutrophils play a key rate in the pathophysiology of septic multiple organ dysfunction syndrome (MODS) through excessive release of toxic granule components and reactive oxygen metabolites with consequent tissue destruction. The increase of senescent neutrophils during sepsis indicates a potential breakdown of autoregulatory mechanisms Including apoptotic processes to remove activated neutrophils from inflammatory sites. Therefore, neutrophil apoptosis of patients with severe sepsis and its regulatory mechanisms were investigated. Spontaneous neutrophil apoptosis from patients with severe sepsis was significantly reduced in comparison to healthy individuals. Cytokines detected in the circulation during sepsis (tumor necrosis factor-alpha [TNF-alpha], interferon-gamma [IFN-gamma], granulocyte colony-stimulating factor [G-CSF], granulocyte-macrophage colony-stimulating factor [GM-CSF]) inhibited neutrophil apoptosis in both groups, though the effect was more distinct in neutrophils from healthy humans. Addition of lipopolysaccharide (LPS) to neutrophils from healthy humans markedly (P