Onose J, Teshima R, Sawada J
Meiji College of Pharmacy, Tokyo, Japan.
Immunol Lett. 1998 Nov;64(1):17-22. doi: 10.1016/s0165-2478(98)00076-5.
The effects of a Ca2(+)-ATPase inhibitor, cyclopiazonic acid (CPA), and two hydroquinone-antioxidants, 2,5-di-(tert-butyl)-1,4-hydroquinone (DTBHQ) and 2,5-di-(tert-amyl)-1,4-hydroquinone (DTAHQ) on the release of IL-4 and MCP-1 from RBL-2H3 cells were investigated. CPA, DTBHQ and DTAHQ, all of which induce intracellular free Ca2+ concentration ([Ca2+]i) increase, induced IL-4 and MCP-1 release in a dose-dependent manner. The release of TNF-alpha required both a Ca2(+)-ATPase inhibitor and 12-O-tetradecanoylphorbol-13-acetate (TPA). However, the Ca2(+)-ATPase inhibitors induced IL-4 and MCP-1 production without TPA. The release of IL-4 and MCP-1 reached a maximum at 9 and 6 h, respectively. IL-4 and MCP-I release was inhibited by treatment with the immunosuppressant FK-506 and actinomycin D. Therefore, in our system IL-4 and MCP-1 release involves Ca2(+)-dependent and FK-506-sensitive signaling pathways. This is the first report about Th-2 type cytokine and chemokine production in RBL-2H3 cells.
研究了钙离子 - ATP酶抑制剂环匹阿尼酸(CPA)以及两种对苯二酚类抗氧化剂2,5 - 二 - (叔丁基)-1,4 - 对苯二酚(DTBHQ)和2,5 - 二 - (叔戊基)-1,4 - 对苯二酚(DTAHQ)对RBL - 2H3细胞释放白细胞介素 - 4(IL - 4)和单核细胞趋化蛋白 - 1(MCP - 1)的影响。CPA、DTBHQ和DTAHQ均可诱导细胞内游离钙离子浓度([Ca2 + ]i)升高,并以剂量依赖的方式诱导IL - 4和MCP - 1的释放。肿瘤坏死因子 - α(TNF - α)的释放既需要钙离子 - ATP酶抑制剂,又需要12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯(TPA)。然而,钙离子 - ATP酶抑制剂在没有TPA的情况下也能诱导IL - 4和MCP - 1的产生。IL - 4和MCP - 1的释放在9小时和6小时时分别达到最大值。用免疫抑制剂FK - 506和放线菌素D处理可抑制IL - 4和MCP - 1的释放。因此,在我们的体系中,IL - 4和MCP - 1的释放涉及钙离子依赖和FK - 506敏感的信号通路。这是关于RBL - 2H3细胞中Th - 2型细胞因子和趋化因子产生的首次报道。