Rey A, M'Rini C, Sozzani P, Lamboeuf Y, Beraud M, Caput D, Ferrara P, Pipy B
Laboratoire Macrophages, Médiateurs de l'Inflammation et Interactions Cellulaires, UPS E.A. 2405, Bâtiment L1, Hôpital de Rangueil, Toulouse, France.
Biochim Biophys Acta. 1998 Aug 28;1393(2-3):244-52. doi: 10.1016/s0005-2760(98)00080-0.
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 cytosolic 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.
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，但不影响由次优浓度的炎性激动剂（调理酵母聚糖）触发的环氧化酶代谢产物的产生。放线菌酮可抑制IL-13的这些作用，提示其涉及从头蛋白质合成。事实上，IL-13可诱导胞质型磷脂酶A2（cPLA2）蛋白和mRNA水平随时间依赖性增加。本研究证明了IL-13通过修饰cPLA2表达及随后的AA动员来调节巨噬细胞炎症过程的新途径。
