IL-13增加小鼠腹膜巨噬细胞炎症过程中cPLA2基因和蛋白的表达以及花生四烯酸的动员

Astrid Rey , Christine M’Rini , Patricia Sozzani , Yves Lamboeuf , Maryse Beraud , Daniel Caput , Pascual Ferrara , Bernard Pipy
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引用次数: 27

摘要

用白细胞介素-13 (IL-13)预处理小鼠腹腔巨噬细胞可增强花生四烯酸(AA)的动员和HETEs的产生,但不影响由炎症激动剂(调理酶)的次优浓度触发的环加氧酶代谢物的产生。环己亚胺抑制了IL-13的这些作用,表明参与了从头蛋白合成。事实上,IL-13诱导细胞生成PLA2 (cPLA2)蛋白和mRNA水平的时间依赖性增加。本研究揭示了IL-13通过改变cPLA2表达和随后的AA动员来调节巨噬细胞炎症过程的新途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
IL-13 increases the cPLA2 gene and protein expression and the mobilization of arachidonic acid during an inflammatory process in mouse peritoneal macrophages

Pretreatment of mouse peritoneal macrophages with interleukin-13 (IL-13) potentiates the mobilization of arachidonic acid (AA) and the production of HETEs but does not affect the production of cyclooxygenase metabolites triggered by the suboptimal concentration of an inflammatory agonist (opsonized-zymosan). Cycloheximide suppresses these effects of IL-13 suggesting that de novo protein synthesis is involved. Indeed, IL-13 induces a time-dependent increase in the levels of cytolosic PLA2 (cPLA2) protein and mRNA. This study demonstrates a new pathway for IL-13 to modulate the inflammatory process in macrophages via modifications of cPLA2 expression and subsequent AA mobilization.

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