Retzlaff C, Yamamoto Y, Hoffman P S, Friedman H, Klein T W
Department of Medical Microbiology and Immunology, University of South Florida College of Medicine, Tampa 33612.
Infect Immun. 1994 Dec;62(12):5689-93. doi: 10.1128/iai.62.12.5689-5693.1994.
Bacterial heat shock proteins (hsp) have been shown to be important immunogens stimulating both T cells and B cells. However, little is known concerning the direct interactions between hsp and macrophages. In this study, we demonstrated that treatment of macrophage cultures with purified bacterial hsp, including Legionella pneumophila hsp60, Escherichia coli GroEL, Mycobacterium tuberculosis hsp70, Mycobacterium leprae hsp65, and Mycobacterium bovis BCG hsp65, increased the steady-state levels of cytokine mRNA for interleukin-1 alpha (IL-1 alpha), IL-1 beta, IL-6, tumor necrosis factor alpha, and granulocyte-macrophage colony-stimulating factor as well as supernatant IL-1 secretion. This effect was shown not to be due to contamination of the hsp preparations with bacterial lipopolysaccharide. However, not all hsp induced cytokines; M. tuberculosis hsp10 showed minimal activity in our study. These results suggest that bacterial hsp might modulate immunity by rapidly and directly increasing cytokine production in macrophages.
细菌热休克蛋白(hsp)已被证明是刺激T细胞和B细胞的重要免疫原。然而,关于hsp与巨噬细胞之间的直接相互作用却知之甚少。在本研究中,我们证明,用纯化的细菌hsp处理巨噬细胞培养物,包括嗜肺军团菌hsp60、大肠杆菌GroEL、结核分枝杆菌hsp70、麻风分枝杆菌hsp65和牛分枝杆菌卡介苗hsp65,可增加白细胞介素-1α(IL-1α)、IL-1β、IL-6、肿瘤坏死因子α和粒细胞-巨噬细胞集落刺激因子的细胞因子mRNA稳态水平以及上清液IL-1分泌。结果表明,这种效应并非由于hsp制剂被细菌脂多糖污染所致。然而,并非所有hsp都能诱导细胞因子产生;在我们的研究中,结核分枝杆菌hsp10的活性最低。这些结果表明,细菌hsp可能通过迅速直接增加巨噬细胞中的细胞因子产生来调节免疫。