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首页> 外文期刊>Infection and immunity >Reversible Lipid Accumulation and Associated Division Arrest of Mycobacterium avium in Lipoprotein-Induced Foamy Macrophages May Resemble Key Events during Latency and Reactivation of Tuberculosis
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Reversible Lipid Accumulation and Associated Division Arrest of Mycobacterium avium in Lipoprotein-Induced Foamy Macrophages May Resemble Key Events during Latency and Reactivation of Tuberculosis

机译：脂蛋白诱导的泡沫巨噬细胞中鸟分枝杆菌的可逆脂质蓄积和相关分裂逮捕可能类似于结核病的潜伏期和再激活期间的关键事件。

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During the dormant phase of tuberculosis, Mycobacterium tuberculosis persists in lung granulomas by residing in foamy macrophages (FM) that contain abundant lipid bodies (LB) in their cytoplasm, allowing bacilli to accumulate lipids as intracytoplasmic lipid inclusions (ILI). An experimental model of FM is presented where bone marrow-derived mouse macrophages are infected with M. avium and exposed to very-low-density lipoprotein (VLDL) as a lipid source. Quantitative analysis of detailed electron microscope observations showed the following results. (i) Macrophages became foamy, and mycobacteria formed ILI, for which host triacylglycerides, rather than cholesterol, was essential. (ii) Lipid transfer occurred via mycobacterium-induced fusion between LB and phagosomes. (iii) Mycobacteria showed a thinned cell wall and became elongated but did not divide. (iv) Upon removal of VLDL, LB and ILI declined within hours, and simultaneous resumption of mycobacterial division restored the number of mycobacteria to the same level as that found in untreated control macrophages. This showed that the presence of ILI resulted in a reversible block of division without causing a change in the mycobacterial replication rate. Fluctuation between ILI either partially or fully extending throughout the mycobacterial cytoplasm was suggestive of bacterial cell cycle events. We propose that VLDL-driven FM constitute a well-defined cellular system in which to study changed metabolic states of intracellular mycobacteria that may relate to persistence and reactivation of tuberculosis.
机译：在结核病的休眠期，结核分枝杆菌通过驻留在细胞质中包含大量脂质体（LB）的泡沫巨噬细胞（FM）中而在肺肉芽肿中持续存在，从而使杆菌以脂质体的形式积聚为胞浆内脂质包裹体（ILI）。提出了FM的实验模型，其中骨髓来源的小鼠巨噬细胞感染了鸟分枝杆菌，并暴露于极低密度脂蛋白（VLDL）作为脂质来源。详细的电子显微镜观察结果的定量分析显示以下结果。 （i）巨噬细胞起泡沫，分枝杆菌形成ILI，对此，宿主甘油三酯而不是胆固醇至关重要。 （ii）通过分枝杆菌诱导的LB和吞噬体之间的融合发生脂质转移。 （iii）分枝杆菌显示细胞壁变薄并变长但不分裂。 （iv）去除VLDL后，LB和ILI在数小时内下降，并且同时恢复分枝杆菌分裂使分枝杆菌的数目恢复到与未处理的对照巨噬细胞相同的水平。这表明ILI的存在导致可逆的分​​裂阻滞而不引起分枝杆菌复制速率的改变。 ILI之间的波动部分或完全延伸到整个分枝杆菌细胞质，提示细菌细胞周期事件。我们建议VLDL驱动的FM构成一个定义明确的细胞系统，在其中研究可能与结核病的持续性和再激活有关的细胞内分枝杆菌代谢状态的改变。

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