Effects of diesel particles on the control of intracellular mycobacterial growth by human macrophages in vitro
Effects of diesel particles on the control of intracellular mycobacterial growth by human macrophages in vitro
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DOI：
10.1111/j.1574-695x.2006.00050.x
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发表时间：
2006-04-01
影响因子：
--
通讯作者：
Soler, P
中科院分区：
文献类型：
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作者：
Bonay, M;Chambellan, A;Soler, P
可能改变巨噬细胞控制分枝杆菌生长的能力的变化可能有利于分枝杆菌感染后保护性肉芽肿内细菌增殖的重新激活。越来越多的证据表明柴油机尾气颗粒物（DEPs）可以抑制巨噬细胞的某些功能，但DEPs是否会改变巨噬细胞的杀分枝杆菌活性尚不清楚。本研究的目的是评估DEPs对人单核吞噬细胞体外杀菌活性的影响。将来自健康供体的人单核细胞在存在或不存在DEP或炭黑颗粒（CBP）的情况下培养3天，然后用表达荧光素酶活性的牛分枝杆菌卡介苗（Mycobacterium bovis bacillus Calmette-Guerin）报告菌株感染。DEP被单核细胞衍生的巨噬细胞迅速内化，没有细胞毒性作用。暴露于DEPs的细胞的杀分枝杆菌活性与在它们不存在或存在CBPs的情况下培养的细胞的杀分枝杆菌活性没有不同。虽然我们的研究仅限于体外人巨噬细胞的杀分枝杆菌活性，但结果表明DEP不会直接影响抗微生物的第一道防线。暴露于DEPs是否会影响针对分枝杆菌感染的适应性免疫应答仍有待确定。
Changes that may modify the capacity of macrophages to control mycobacterial growth could favour the reactivation of bacillary proliferation within protective granulomas developed in response to mycobacterial infection. There is increasing evidence that diesel exhaust particles (DEPs) could suppress some macrophage functions, but it is not known whether DEPs may alter macrophage mycobactericidal activity. The aim of this study was to assess the effect of DEPs on the mycobactericidal activity of human mononuclear phagocytes in vitro. Human monocytes from healthy donors were cultured for 3 days in the presence or absence of DEPs or carbon black particles (CBPs), and then infected with a Mycobacterium bovis bacillus Calmette-Guerin reporter strain expressing luciferase activity. DEPs were rapidly internalized by monocyte-derived macrophages without cytotoxic effect. Mycobactericidal activity of cells exposed to DEPs was not different from that of cells cultured in their absence or in the presence of CBPs. Although our study was restricted to the mycobactericidal activity of human macrophages in vitro, the results indicate that DEPs do not directly influence the first line of defence against microorganisms. Whether exposure to DEPs influences the adaptive immune response against mycobacterial infections remains to be determined.