Mycobacterium tuberculosis invades and replicates within type II alveolar cells
Mycobacterium tuberculosis invades and replicates within type II alveolar cells
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DOI：
10.1128/iai.64.4.1400-1406.1996
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发表时间：
1996-04-01
影响因子：
3.1
通讯作者：
Goodman, J
中科院分区：
文献类型：
--
作者：
Bermudez, LE;Goodman, J
虽然假设结核分枝杆菌以气溶胶形式吸入肺部后主要感染肺泡巨噬细胞，但假设结核分枝杆菌在到达肺泡间隙时可以与肺泡上皮细胞接触是合理的，因此，作为研究结核分枝杆菌与肺泡上皮细胞相互作用的第一步，我们在体外检测了结核分枝杆菌与肺泡上皮细胞的结合和侵袭能力，将结核分枝杆菌H37Rv和H37Ra菌株培养至中期，并进行粘附和侵袭试验，将A549人II型肺泡细胞系培养融合在添加5%胎牛血清、l -谷氨酰胺和非必需氨基酸的RPMI 1640中，H37Rv比H37Ra、鸟分枝杆菌H37Ra更有效地进入A549细胞。和大肠杆菌HB101 nonpiliated拉伤(4.7% + / - 1.0%的初始接种体与3.1%相比,2 h + / - 0.8%, 2.1% + / - 0.9%,和0.03% + / - 0.0%),入侵更有效的在37摄氏度比在30摄氏度(4.7% + / - 1.0%与2.3% + / - 0.8%)相比,H37Rv和H37Ra都能够繁殖细胞类似的比率高于4天,绑定被anti-CD51抗体抑制55.7% (antivitronectin受体),抗cd29抗体（β(1)整合素）和两种抗体一起使用时，H37Rv的摄取是微管和微丝依赖性的，在10 μ M秋水仙碱和3 μ M细胞松弛素D的存在下，H37Rv的摄取被抑制了61.4%，而在3 μ M细胞松弛素D的存在下，H37Rv的摄取被抑制了72.3%。我们的研究结果表明，结核分枝杆菌能够侵袭II型肺泡上皮细胞，并提出肺泡上皮细胞侵袭与肺部感染发病机制相关的可能性。
Although Mycobacterium tuberculosis is assumed to infect primarily alveolar macrophages after being aspirated into the lung in aerosol form, it is plausible to hypothesize that M. tuberculosis can come in contact with alveolar epithelial cells upon arrival into the alveolar space, Therefore, as a first step toward investigation of the interaction between M. tuberculosis and alveolar epithelial cells, we examined the ability of M. tuberculosis to bind to and invade alveolar epithelial cells in vitro, The H37Rv and H37Ra strains of M. tuberculosis were cultured to mid-log phase and used in both adherence and invasion assays, The A549 human type II alveolar cell line was cultured to confluence in RPMI 1640 supplemented with 5% fetal bovine serum, L-glutamine, and nonessential amino acids, H37Rv was more efficient in entering A549 tells than H37Ra, Mycobacterium avium, and Escherichia coli HB101, a nonpiliated strain (4.7% +/- 1.0% of the initial inoculum in 2 h compared with 3.1% +/- 0.8%, 2.1% +/- 0.9%, and 0.03% +/- 0.0%, respectively), The invasion was more efficient at 37 degrees C than at 30 degrees C (4.7% +/- 1.0% compared with 2.3% +/- 0.8%), H37Rv and H37Ra were both capable of multiplying intracellularly at a similar ratio over 4 days, Binding was inhibited up to 55.7% by anti-CD51 antibody (antivitronectin receptor), up to 55% with anti-CD29 antibody (beta(1) integrin), and 79% with both antibodies used together, Uptake of M. tuberculosis H37Rv was microtubule and microfilament dependent, It was inhibited by 61.4% in the presence of 10 mu M colchicine and by 72.3% in the presence of 3 mu M cytochalasin D, suggesting two separate pathways for uptake, Our results show that M. tuberculosis is capable of invading type II alveolar epithelial cells and raise the possibility that invasion of alveolar epithelial cells is associated with the pathogenesis of lung infection.