Denis M
Pulmonary Research Unit, Faculty of Medicine, University of Sherbrooke, Canada.
Clin Exp Immunol. 1994 Oct;98(1):123-7. doi: 10.1111/j.1365-2249.1994.tb06617.x.
Human bronchoalveolar lavage (BAL) macrophages were obtained from normal human volunteers and infected with an AIDS-associated strain of Mycobacterium avium. Infected cells were exposed to purified envelope glycoprotein (gp120) from HIV-1 or to the recombinant non-glycosylated gp120 fragments PBI-RF and PBI-IIIB. Native gp120 increased Myco. avium growth in human cells from six separate donors, whereas the non-glycosylated fragments of gp120 had no such effect. Moreover, gp120 induced a substantial secretion of prostaglandin E2 (PGE2) from macrophages; inclusion of indomethacin blocked the enhanced permissiveness of infected cells treated with gp120. Soluble CD4 also neutralized the effect of gp120. Overall, these results indicate a role for gp120 in the susceptibility of AIDS patients to Myco. avium infections, mediated by an enhanced PGE2 release.
人支气管肺泡灌洗(BAL)巨噬细胞取自正常人类志愿者,并感染了与艾滋病相关的鸟分枝杆菌菌株。将感染的细胞暴露于来自HIV-1的纯化包膜糖蛋白(gp120)或重组非糖基化gp120片段PBI-RF和PBI-IIIB。天然gp120增加了来自六个不同供体的人细胞中鸟分枝杆菌的生长,而gp120的非糖基化片段则没有这种作用。此外,gp120诱导巨噬细胞大量分泌前列腺素E2(PGE2);加入吲哚美辛可阻断用gp120处理的感染细胞增强的易感性。可溶性CD4也中和了gp120的作用。总体而言,这些结果表明gp120在艾滋病患者对鸟分枝杆菌感染的易感性中起作用,这是由增强的PGE2释放介导的。