Robinson Cory M, Nau Gerard J
Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261, USA.
J Infect Dis. 2008 Aug 1;198(3):359-66. doi: 10.1086/589774.
Mycobacterium tuberculosis is an intracellular pathogen that persists within macrophages and remains a considerable global threat to human health. The purpose of this study was to investigate how interleukin (IL)-12 and IL-27 regulate human macrophage interactions with M. tuberculosis. Quantitative measurement of transcripts showed that IL-12 or M. tuberculosis induced IL-27 gene expression in human macrophages. Furthermore, IL-27 receptor subunits were shown by reverse transcription-polymerase chain reaction and flow cytometry to be expressed and present at the cell surface. Neutralization of IL-27 in the presence of IL-12 reduced viable M. tuberculosis recovered from macrophages. Antimycobacterial activity was accompanied by a heightened inflammatory response that included tumor necrosis factor, IL-6, interferon-gamma, and a subset of chemokines. These results implicate IL-12 and IL-27 in regulating human macrophages, and IL-27 derived from macrophages during infection impedes control of M. tuberculosis growth.
结核分枝杆菌是一种细胞内病原体，它在巨噬细胞内持续存在，仍然是对人类健康的一个相当大的全球威胁。本研究的目的是调查白细胞介素（IL）-12和IL-27如何调节人类巨噬细胞与结核分枝杆菌的相互作用。转录本的定量测量显示，IL-12或结核分枝杆菌可诱导人类巨噬细胞中IL-27基因表达。此外，通过逆转录-聚合酶链反应和流式细胞术显示，IL-27受体亚基在细胞表面表达并存在。在IL-12存在的情况下中和IL-27可减少从巨噬细胞中回收的活结核分枝杆菌。抗分枝杆菌活性伴随着炎症反应增强，包括肿瘤坏死因子、IL-6、干扰素-γ和一部分趋化因子。这些结果表明IL-12和IL-27参与调节人类巨噬细胞，并且感染期间巨噬细胞衍生的IL-27会阻碍对结核分枝杆菌生长的控制。
