Pertussis toxin and H-7 distinguish mechanisms involved in eicosanoid release from lipopolysaccharide-primed macrophages. Eicosanoid release from lipopolysaccharide-primed macrophages.
Pertussis toxin and H-7 distinguish mechanisms involved in eicosanoid release from lipopolysaccharide-primed macrophages. Eicosanoid release from lipopolysaccharide-primed macrophages.
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百日咳毒素和 H-7 区分了脂多糖引发的巨噬细胞释放类二十烷酸的机制。
DOI：
10.1111/j.1432-1033.1990.tb15342.x
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Cottam,GL
中科院分区：
文献类型：
--
作者：
Matsunaga,A;Miller,BC;Cottam,GL
巨噬细胞释放类二十烷酸是对炎症和细菌感染的重要反应。在低浓度下，细菌脂多糖（1-2 μg/ml）不能刺激腹膜巨噬细胞释放类二十烷，但在钙离子载体A23187 （0.1 μM）或蛋白激酶c活化剂12 -肉豆酸酯13 -醋酸酯（50 nM）的刺激下，巨噬细胞释放类二十烷的能力大大增强。在A23187刺激下抑制环加氧酶和脂加氧酶产物的释放。以12 -肉豆蔻酸13 -醋酸磷刺激巨噬细胞时，百日咳毒素处理对类二十烷酸释放无影响。1‐（5‐异喹啉基磺酰基）‐2‐甲基哌嗪（H‐7）是一种有效的蛋白激酶C抑制剂，在脂多糖启动和随后的刺激过程中，当12‐肉豆酸酯13‐乙酸磷作为刺激时，它的存在显著抑制了类二十烷的释放，但不影响A23187刺激的类二十烷的释放。基于这些结果，至少有两种机制参与了脂多糖激活的巨噬细胞对A23187和phorbol 12 -肉豆酸酯13 -醋酸酯的类二十烷酸分泌，这两种机制在百日咳毒素敏感、鸟嘌呤-核苷酸结合蛋白和蛋白激酶C的敏感性上存在明显差异。
Release of eicosanoids is an important response of macrophages to inflammation and bacterial infection. At low concentrations, bacterial lipopolysaccharide (1–2 μg/ml) fails to stimulate eicosanoid release in resident peritoneal macrophages but primes the macrophages for a greatly enhanced release of eicosanoids on stimulation with the calcium ionophore A23187 (0.1 μM) or with phorbol 12‐myristate 13‐acetate (50 nM), an activator of protein kinase C. Incubation of macrophages withBordetella pertussistoxin, prior to priming with lipopolysaccharide, inhibited the release of both cyclooxygenase and lipoxygenase products upon A23187 stimulation. Pertussis toxin treatment of macrophages had no effect on eicosanoid release when the stimulus was phorbol 12‐myristate 13‐acetate. The presence of 1‐(5‐isoquinolinylsulfonyl)‐2‐methylpiperazine (H‐7), an effective inhibitor of protein kinase C, during lipopolysaccharide priming and subsequent stimulation significantly inhibited eicosanoid release when phorbol 12‐myristate 13‐acetate was the stimulus, but did not affect eicosanoid release stimulated by A23187. Based on these results, at least two mechanisms, distinguished by apparent differences in sensitivity to pertussis‐toxin‐sensitive, guanine‐nucleotide‐binding proteins and protein kinase C, are involved in eicosanoid secretion by lipopolysaccharide‐activated macrophages in response to A23187 and phorbol 12‐myristate 13‐acetate.
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DOI：
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