Platelet-activating factor augments tumor necrosis factor and procoagulant activity.
Platelet-activating factor augments tumor necrosis factor and procoagulant activity.
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血小板激活因子增强肿瘤坏死因子和促凝血活性。
DOI：
10.1016/0022-4804(92)90083-c
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Fletcher,JR
中科院分区：
文献类型：
--
作者：
Maier,RV;Hahnel,GB;Fletcher,JR
血小板活化因子（PAF）的输注再现了宿主对内毒素血症和脓毒症的生理反应。肿瘤坏死因子（TNF）和促凝血活性（PCA）是由组织固定的巨噬细胞（Mφ）大量产生的另外两种潜在有害的中枢炎症介质。PAF与TNF或PCA产生之间的关系（如果有的话）尚不清楚。分别用PAF和内毒素（LPS）处理兔肺泡Mφ。PAF对Mφ PCA和TNF无影响。PAF（10−9−10− 6 M）联合治疗可使Mφ PCA和TNF水平升高，剂量反应比单独LPS治疗高2 - 6倍。PAF（10− 6 M）预处理T-4 ~-6 h的Mφ，可使TNF和PCA水平增加8 ~ 9倍。因此，在LPS刺激前，用PAF与Mφ共孵育和预处理或“引发”Mφ可大大增加Mφ产生PCA和TNF。增加这两种强效炎症介质产生的能力可能部分解释了PAF在体内的作用机制。
Infusion of platelet activating factor (PAF) reproduces the host physiologic response to endotoxemia and sepsis. Tumor necrosis factor (TNF) and procoagulant activity (PCA) are two other potentially deleterious central inflammatory mediators produced in large quantities by tissue-fixed macrophages (Mφ). The relationship, if any, between PAF and TNF or PCA production is unknown. Rabbit alveolar Mφ were treatedin vitrowith PAF alone and prior to endotoxin (LPS). PAF alone had no effect on Mφ PCA or TNF. PAF (10−9−10−6M) cotreatment enhanced Mφ PCA and TNF levels in a dose response from two- to sixfold above that of LPS treatment alone. PAF (10−6M) pretreatment of Mφ at T -4 to -6 hr produces an eight- to ninefold enhancement in both TNF and PCA levels. Thus, both coincubation and pretreatment or “priming” of the Mφ with PAF prior to LPS stimulation greatly increase Mφ production of PCA and TNF. The ability to augment the production of these two potent inflammatory mediators may explain in part the mechanism of action of PAFin vivo.