Denis M, Ghadirian E
Pulmonary Research Unit, Faculty of Medicine, University of Sherbrooke, Canada.
Clin Exp Immunol. 1994 Jul;97(1):76-82. doi: 10.1111/j.1365-2249.1994.tb06582.x.
The complex interaction between HIV-1 infection and Mycobacterium avium was studied. Viral burden was assessed, as well as immune response to HIV-1 in the context of Myco. avium infections. We also examined serum cytokine levels and cytokine release by blood mononuclear cells in HIV-1-infected subjects, infected or not with Myco. avium. Undetectable serum levels of IL-1, tumour necrosis factor-alpha (TNF-alpha) and IL-6 were found in normal controls and in groups I, II and III of HIV-1-infected subjects. Moderate levels of TNF-alpha, IL-1 and IL-6 were found in the sera of group IV patients. When group IV was subdivided into subjects with and without Myco. avium infections, subjects with Myco, avium infections were shown to have higher serum levels of TNF-alpha, IL-1 beta and IL-6 than those with other infections. Blood mononuclear cells from controls and HIV subjects were stimulated with bacterial lipopolysaccharide, and cytokine levels assessed. Cells from group II patients were shown to secrete normal levels of TNF-alpha and IL-6, and lower levels of IL-1 beta; group III subjects released higher levels of IL-6. Patients in group IV had blood cells that released elevated levels of IL-6 and TNF-alpha, and lower levels of IL-1 beta. Group IV subjects with Myco. avium infections had blood cells that released higher levels of TNF-alpha, IL-6 and IL-1 than group IV subjects with other infections. Assessment of viral burden in cells of HIV-1-infected subjects revealed that Myco. avium-infected subjects had a higher level of virus burden and a lower level of lymphoproliferative response to an inactivated gp120-depleted HIV-1 antigen than AIDS subjects with other infections. These data suggest that Myco. avium infections in HIV-1-infected subjects hasten the progression of viral disease, enhance cytokine release and contribute to the anergy to viral antigens.
研究了HIV-1感染与鸟分枝杆菌之间的复杂相互作用。评估了病毒载量以及在鸟分枝杆菌感染背景下对HIV-1的免疫反应。我们还检测了HIV-1感染受试者(无论是否感染鸟分枝杆菌)的血清细胞因子水平以及血液单核细胞释放的细胞因子。在正常对照组以及HIV-1感染受试者的I、II和III组中,未检测到血清白细胞介素-1(IL-1)、肿瘤坏死因子-α(TNF-α)和IL-6水平。在IV组患者的血清中发现了中等水平的TNF-α、IL-1和IL-6。当将IV组细分为有和没有鸟分枝杆菌感染的受试者时,发现有鸟分枝杆菌感染的受试者血清中TNF-α、IL-1β和IL-6水平高于其他感染的受试者。用细菌脂多糖刺激对照组和HIV受试者的血液单核细胞,并评估细胞因子水平。II组患者的细胞分泌正常水平的TNF-α和IL-6,IL-1β水平较低;III组受试者释放较高水平的IL-6。IV组患者的血细胞释放升高水平的IL-6和TNF-α,IL-1β水平较低。有鸟分枝杆菌感染的IV组受试者的血细胞释放的TNF-α、IL-6和IL-1水平高于有其他感染的IV组受试者。对HIV-1感染受试者细胞中的病毒载量评估显示,与有其他感染的艾滋病受试者相比,有鸟分枝杆菌感染的受试者病毒载量水平更高,对灭活的gp120缺失型HIV-1抗原的淋巴细胞增殖反应水平更低。这些数据表明,HIV-1感染受试者中的鸟分枝杆菌感染加速了病毒性疾病的进展,增强了细胞因子释放,并导致对病毒抗原的无反应性。