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鼠伤寒沙门氏菌孔蛋白诱导的细胞因子释放

Release of cytokines induced by Salmonella typhimurium porins.

作者信息

Galdiero F, de L'ero G C, Benedetto N, Galdiero M, Tufano M A

机构信息

Microbiology Institute, First Medical School, University of Naples, Italy.

出版信息

Infect Immun. 1993 Jan;61(1):155-61. doi: 10.1128/iai.61.1.155-161.1993.

Abstract

Salmonella typhimurium SH5014 porins induce the release of tumor necrosis factor alpha (TNF-alpha), interleukin 1 alpha (IL-1 alpha), and IL-6 by human monocytes and of gamma interferon (IFN-gamma) and IL-4 by human lymphocytes. Porins at 1 microgram/ml induce the greatest release of TNF-alpha, IL-1 alpha, and IL-6 by monocytes and of IL-4 by lymphocytes, while porins at 5 micrograms/ml induce the greatest release of IFN-gamma by lymphocytes. The R form of lipopolysaccharide (LPS-R) induces the greatest release of TNF-alpha and IL-1 alpha by monocytes when used at a low concentration (1 microgram/ml). At higher concentrations (5 and 10 micrograms/ml, respectively), LPS-R induces the maximal release of IL-6 from monocytes and the maximal release of IL-4 from lymphocytes. The S form of LPS (LPS-S) induces the greatest release of TNF-alpha, IL-1 alpha, and IL-6 by monocytes and that of IL-4 by lymphocytes when used at a concentration of 1 microgram/ml. After stimulation with LPS-S, the largest quantity of TNF-alpha and IL-1 alpha released was less than that obtained after stimulation with LPS-R at the same concentration, while the quantity of IL-6 released was found to be slightly higher than that obtained after stimulation with porins or LPS-R. LPS-S (1 microgram/ml) induces IFN-gamma release from lymphocytes in notably smaller quantities than that obtained with LPS-R and slightly larger quantities than that obtained with porins. The preparation of porins used was found to be contaminated with 10 pg of LPS per 10 micrograms of porins, a quantity which was found to have no biological effect; furthermore, porin preparations with the addition of polymyxin B gave the same results.

摘要

鼠伤寒沙门氏菌SH5014孔蛋白可诱导人单核细胞释放肿瘤坏死因子α(TNF-α)、白细胞介素1α(IL-1α)和IL-6,以及人淋巴细胞释放γ干扰素(IFN-γ)和IL-4。1微克/毫升的孔蛋白可诱导单核细胞释放最多的TNF-α、IL-1α和IL-6,以及淋巴细胞释放最多的IL-4,而5微克/毫升的孔蛋白可诱导淋巴细胞释放最多的IFN-γ。低浓度(1微克/毫升)使用时,脂多糖的R型(LPS-R)可诱导单核细胞释放最多的TNF-α和IL-1α。在较高浓度(分别为5和10微克/毫升)时,LPS-R可诱导单核细胞释放最大量的IL-6以及淋巴细胞释放最大量的IL-4。脂多糖的S型(LPS-S)在浓度为1微克/毫升时,可诱导单核细胞释放最多的TNF-α、IL-1α和IL-6,以及淋巴细胞释放最多的IL-4。用LPS-S刺激后,释放的TNF-α和IL-1α的最大量低于相同浓度下用LPS-R刺激后获得的量,而发现释放的IL-6的量略高于用孔蛋白或LPS-R刺激后获得的量。LPS-S(1微克/毫升)诱导淋巴细胞释放IFN-γ的量明显少于用LPS-R诱导的量,略多于用孔蛋白诱导的量。所使用的孔蛋白制剂被发现每10微克孔蛋白污染有10皮克的LPS,这一量被发现没有生物学效应;此外,添加多粘菌素B的孔蛋白制剂给出了相同的结果。

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