15-脱氧-Δ(12,14)-前列腺素J2抑制巨噬细胞产生白细胞介素-10和白细胞介素-12。
15-Deoxy-delta(12,14)-prostaglandin J(2) inhibits IL-10 and IL-12 production by macrophages.
作者信息
Azuma Y, Shinohara M, Wang P L, Ohura K
机构信息
Department of Pharmacology, Osaka Dental University, 8-1 Kuzuhahanazono-cho, Osaka, Hirakata, 573-1121, Japan.
出版信息
Biochem Biophys Res Commun. 2001 May 4;283(2):344-6. doi: 10.1006/bbrc.2001.4783.
15-Deoxy-Delta(12,14)-prostaglandin J(2) (dPGJ(2)) is a metabolite of prostaglandin D(2), that binds to peroxisome proliferator-activated receptor gamma (PPARgamma). PPARgamma and prostaglandin D(2) synthase, which is required for dPGJ(2) synthesis, are predominantly expressed in macrophages. In contrast, IL-10 and IL-12 produced by macrophages stimulate Th1 and Th2 immune response, respectively. This study investigated the effect of dPGJ(2) on IL-10 and IL-12 production by macrophages in response to lipopolysaccharide (LPS). Our data clearly demonstrated that dPGJ(2) inhibits LPS-induced IL-10 and IL-12 production by macrophages. A different agonist of PPARgamma, 13-hydroxyoctadecadienoic acid, similarly inhibited the production of IL-10 and IL-12 in response to LPS. Further, dPGJ(2) did not appear to act through the PGD(2) receptor. These results suggest that dPGJ(2) may inhibit LPS-induced IL-10 and IL-12 production by macrophages through PPARgamma.
15-脱氧-Δ（12,14）-前列腺素J2（dPGJ2）是前列腺素D2的一种代谢产物，它能与过氧化物酶体增殖物激活受体γ（PPARγ）结合。PPARγ以及dPGJ2合成所需的前列腺素D2合酶主要在巨噬细胞中表达。相比之下，巨噬细胞产生的白细胞介素-10（IL-10）和白细胞介素-12（IL-12）分别刺激Th1和Th2免疫反应。本研究调查了dPGJ2对巨噬细胞响应脂多糖（LPS）产生IL-10和IL-12的影响。我们的数据清楚地表明，dPGJ2可抑制LPS诱导的巨噬细胞产生IL-10和IL-12。PPARγ的另一种激动剂13-羟基十八碳二烯酸同样抑制了巨噬细胞响应LPS产生IL-10和IL-12。此外，dPGJ2似乎并非通过前列腺素D2受体发挥作用。这些结果表明，dPGJ2可能通过PPARγ抑制LPS诱导的巨噬细胞产生IL-10和IL-12。
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