Effects of endotoxins and cytokines on the secretion of platelet-activating factor-acetylhydrolase by human decidual macrophages.
Effects of endotoxins and cytokines on the secretion of platelet-activating factor-acetylhydrolase by human decidual macrophages.
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DOI：
10.1210/jcem.77.5.7521345
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发表时间：
1993-09
影响因子：
9.8
通讯作者：
Hisashi Narahara;Yuichi Nishioka;John M. Johnston
中科院分区：
文献类型：
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作者：
Hisashi Narahara;Yuichi Nishioka;John M. Johnston
目的探讨血小板活化因子在分娩、早产和胎膜早破中的作用。研究设计通过酶消化、Ficoll-Paque离心或流式细胞术分选获得蜕膜巨噬细胞群。内毒素和细胞因子对这些细胞分泌血小板活化因子乙酰水解酶的影响进行了研究。结果脂多糖抑制蜕膜巨噬细胞分泌血小板活化因子乙酰水解酶。白细胞介素-1受体拮抗剂或白细胞介素-1 α、白细胞介素-1 β或肿瘤坏死因子-α的中和抗体可部分逆转抑制作用。肿瘤坏死因子-α、白细胞介素-1 α和白细胞介素-1 β也降低了酶的分泌。肿瘤坏死因子-α和白细胞介素-1 β的抑制作用被相应的抗体特异性中和。白细胞介素1受体拮抗剂可阻断白细胞介素1 α或白细胞介素1 β对分泌的影响。结论血小板活化因子参与了内毒素引起的早产或胎膜早破的发病机制及细胞因子网络的激活。
OBJECTIVE The aim was to clarify the role of platelet-activating factor in parturition, preterm labor, and premature rupture of membranes. STUDY DESIGN Decidual macrophage populations were obtained by enzymic digestion, Ficoll-Paque centrifugation, or flow cytometric sorting. The effects of endotoxins and cytokines on platelet-activating factor-acetylhydrolase secretion by these cells were examined. RESULTS Lipopolysaccharide inhibited the platelet-activating factor-acetylhydrolase secretion by decidual macrophages. The inhibition was partially reversed by interleukin-1 receptor antagonist or by neutralizing antibodies against interleukin-1 alpha, interleukin-1 beta, or tumor necrosis factor-alpha. Tumor necrosis factor-alpha, interleukin-1 alpha, and interleukin-1 beta also decreased the enzyme secretion. The inhibitory actions of tumor necrosis factor-alpha and interleukin-1 beta were specifically neutralized by the corresponding antibodies. The effect of interleukin-1 alpha or interleukin-1 beta on the secretion was abolished by interleukin-1 receptor antagonist. CONCLUSION It is suggested that platelet-activating factor is involved in the pathogenesis of preterm labor or premature rupture of membranes caused by endotoxins and the subsequent activation of cytokine network.