美国哈佛大学医学院一项最新研究显示，艾滋病病毒携带者之所以易感染结核杆菌，是因为病毒破坏了人体抵抗结核杆菌的防御体系，这对预防艾滋病和结核病双重感染的研究具有重要意义。
研究人员将健康人与尚未出现结核病症状的艾滋病病毒携带者进行对比研究发现，两者的肺泡巨噬细胞存在差异，艾滋病病毒携带者的对结核杆菌的免疫反应水平较低。
研究人员随后采取了艾滋病病毒携带者的肺部样本，发现其中一种名为IL－10的分子水平有所升高。肺泡巨噬细胞抵抗结核杆菌的能力降低，正是IL－10增多的结果，因为它导致肺泡巨噬细胞中蛋白质BCL－3量减少。
这项研究成果刊登在新一期《白细胞生物学杂志》上。该杂志副主编约翰·惠里认为，艾滋病病毒和结核杆菌是人类在公共卫生领域面临的严峻挑战，二者结合后危害性尤其严重，哈佛大学的研究增进了人类对这种双重感染的了解。
世界卫生组织的相关资料显示，并发结核病是艾滋病患者死亡的常见原因。（生物谷Bioon.com）
生物谷推荐原始出处：
Journal of Leukocyte Biology. 2009;86:53-60.
Impaired M. tuberculosis-mediated apoptosis in alveolar macrophages from HIV+ persons: potential role of IL-10 and BCL-3
Naimish R. Patel1, Katharine Swan, Xin Li, Souvenir D. Tachado and Henry Koziel
Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
1. Correspondence: Pulmonary, Critical Care and Sleep Medicine, BIDMC, Kirstein Hall, Room KSB-23, 330 Brookline Ave., Boston, MA 02215, USA.
The mechanism of increased MTb disease susceptibility in HIV+ persons remains poorly understood. Apoptosis of macrophages in response to MTb represents a critical host defense response, and decreased apoptosis may represent a mechanism of increased susceptibility to MTb in HIV. In the current study, MTb-mediated apoptosis of human AM was reduced in HIV+ subjects compared with healthy subjects in a TNF--dependent manner. IL-10 levels in BALF from HIV+ persons were significantly elevated compared with HIV– persons, and exogenous IL-10 reduced MTb-mediated apoptosis in healthy AM, suggesting that IL-10 could mediate decreased apoptosis observed in HIV. Further study showed that IL-10 reduced TNF release in response to MTb in AM through a reduction in TNF mRNA levels, and exogenous TNF could partially reverse IL-10-associated effects on AM apoptosis. IL-10 did not influence p-IRAK, IB degradation, or NF-B p65 nuclear translocation in response to MTb, but IL-10 did increase levels of AM BCL-3, an inhibitor of NF-B nuclear activity. BCL-3 knockdown in human macrophages increased MTb-mediated TNF release. Importantly, BCL-3 levels in AM from HIV+ subjects were higher compared with healthy subjects. Taken together, these data suggest that elevated lung levels of IL-10 may impair MTb-mediated AM apoptosis in HIV through a BCL-3-dependent mechanism. BCL-3 may represent a potential therapeutic target to treat or prevent MTb disease in HIV+ persons.
