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志贺氏菌感染中与抗干扰素-γ抗体相关的死菌诱导的细胞因子释放

Cytokine release induced by killed bacteria associated with anti-IFN-gamma antibody in Shigella infection.

作者信息

Sinha A K, Bagchi A K

机构信息

Division of Immunology and Vaccine Development (R-412), National Institute of Cholera & Enteric Diseases, P-33, CIT Road, Scheme XM, Beliaghata, Kolkata 10, India.

出版信息

Cytokine. 2005 Jul 21;31(2):87-93. doi: 10.1016/j.cyto.2005.03.004.

Abstract

An effort was made to analyze the effect of in vitro stimulation on macrophages using killed Shigella dysenteriae type-1 (KSD1) coupled with anti-Interferon Gamma (anti-IFN-gamma) antibody. The stimulated macrophages were co-cultured with primed or non-primed T-cells from Shigella infected patients. T-cell cultures were also established by co-culturing KSD1 coupled with or without PHA stimulated macrophages. Emulsified KSD1 coupled with anti-IFN-gamma antibody was found to act as a potent immunogen, inducing the release of Th1 cytokine from primed T-cells cultured in acute stage of the disease. It was observed that the levels of IFN-gamma and IL-2 production rather than IL-4 and IL-6 were increased as the disease became more severe. On comparison, the subsequent values of IL-6, IFN-gamma, IL-4 and IL-2 were found to be less significant in healthy primed T-cell cultures. This was also associated with a substantial production of superoxide ions (O2-), which probably inhibits the colonization of intracellular Shigella due to the presence of anti-IFN-gamma antibodies. On the other hand KSD1 with or without PHA failed to induce such responses. The above findings reflect that in the presence of anti-IFN-gamma antibody, KSD1 acts as a potential immunogen for eliciting cellular immunity against shigellosis.

摘要

本研究旨在分析用灭活的1型痢疾志贺菌(KSD1)结合抗γ干扰素(anti-IFN-γ)抗体对巨噬细胞进行体外刺激的效果。将受刺激的巨噬细胞与来自志贺菌感染患者的致敏或未致敏T细胞共培养。还通过将KSD1与PHA刺激或未刺激的巨噬细胞共培养来建立T细胞培养体系。结果发现,乳化的KSD1结合抗IFN-γ抗体可作为一种有效的免疫原,能诱导疾病急性期培养的致敏T细胞释放Th1细胞因子。研究观察到,随着疾病加重,IFN-γ和IL-2的产生水平升高,而IL-4和IL-6的产生水平未升高。相比之下,在健康的致敏T细胞培养体系中,IL-6、IFN-γ、IL-4和IL-2的后续值则不那么显著。这也与超氧阴离子(O2-)的大量产生有关,由于抗IFN-γ抗体的存在,超氧阴离子可能会抑制细胞内志贺菌的定植。另一方面,无论有无PHA,KSD1均未能诱导出此类反应。上述研究结果表明,在抗IFN-γ抗体存在的情况下,KSD1可作为一种潜在的免疫原,引发针对志贺菌病的细胞免疫。

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