DP受体激动剂治疗后巨噬细胞自然免疫相关功能改变的同时测定

Kiyoshi Daito, Y. Azuma, M. Daito, K. Ohura
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引用次数: 2

摘要

前列腺素D2 (PGD2)通过腺苷环化酶偶联受体作用于PGD2 (DP受体)。本研究表明,DP受体激动剂BW245C可调节与自然免疫相关的巨噬细胞功能。BW245C在0.1 ~ 10μM浓度下抑制巨噬细胞趋化,在10μM浓度下抑制巨噬细胞对大肠杆菌的吞噬。此外,BW245C在0.1 ~ 10μM浓度下抑制pma刺激巨噬细胞产生超氧阴离子,在10μM浓度下抑制lps刺激巨噬细胞产生亚硝酸盐。相比之下,BW245C在lps刺激的巨噬细胞浓度为1至10μM时,可增强促炎细胞因子TNF-α的产生。这些结果提示PGD2可能通过DP受体调节巨噬细胞与自然免疫相关的功能。
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Simultaneous Determination of Alteration of a Variety of Macrophage Functions Related to Natural Immunity Following Treatment with a DP Receptor Agonist
Prostaglandin D2 (PGD2) acts via the adenyl cyclase-coupled receptor for PGD2 (DP receptor). Here we present evidence that BW245C, a DP receptor agonist, modulates macrophage functions related to natunal immunity. BW245C inhibited macrophage chemotaxis at concentrations of 0.1 to 10μM and phagocytosis of Escherichia coli by macrophages at a concentration of 10μM. In addition, BW245C inhibited the production of superoxide anions by PMA-stimulated macrophages at concentrations of 0.1 to 10μM and nitrite production by LPS-stimulated macrophages at a concentration of 10μM. In contrast, BW245C potentiated the production of TNF-α, a pro-inflammatory cytokine, by LPS-stimulated macrophages at concentrations of 1 to 10μM. These results suggest that PGD2 may modulate macrophage functions related to natural immunity via the DP receptor.
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