美國哈佛大學(xué)醫(yī)學(xué)院一項最新研究顯示,，艾滋病病毒攜帶者之所以易感染結(jié)核桿菌，是因為病毒破壞了人體抵抗結(jié)核桿菌的防御體系,，這對預(yù)防艾滋病和結(jié)核病雙重感染的研究具有重要意義,。
研究人員將健康人與尚未出現(xiàn)結(jié)核病癥狀的艾滋病病毒攜帶者進行對比研究發(fā)現(xiàn)，兩者的肺泡巨噬細胞存在差異,，艾滋病病毒攜帶者的對結(jié)核桿菌的免疫反應(yīng)水平較低,。
研究人員隨后采取了艾滋病病毒攜帶者的肺部樣本，發(fā)現(xiàn)其中一種名為IL－10的分子水平有所升高,。肺泡巨噬細胞抵抗結(jié)核桿菌的能力降低,，正是IL－10增多的結(jié)果，因為它導(dǎo)致肺泡巨噬細胞中蛋白質(zhì)BCL－3量減少,。
這項研究成果刊登在新一期《白細胞生物學(xué)雜志》上,。該雜志副主編約翰·惠里認為，艾滋病病毒和結(jié)核桿菌是人類在公共衛(wèi)生領(lǐng)域面臨的嚴峻挑戰(zhàn),，二者結(jié)合后危害性尤其嚴重,，哈佛大學(xué)的研究增進了人類對這種雙重感染的了解。
世界衛(wèi)生組織的相關(guān)資料顯示，并發(fā)結(jié)核病是艾滋病患者死亡的常見原因,。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
