Institute of Medical Microbiology and Hospital Hygiene, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
PLoS One. 2013;8(1):e54219. doi: 10.1371/journal.pone.0054219. Epub 2013 Jan 11.
Mycoplasma hominis is a facultative human pathogen primarily associated with bacterial vaginosis and pelvic inflammatory disease, but it is also able to spread to other sites, leading to arthritis or, in neonates, meningitis. With a minimal set of 537 annotated genes, M. hominis is the second smallest self-replicating mycoplasma and thus an ideal model organism for studying the effects of an infectious agent on its host more closely. M. hominis adherence, colonisation and invasion of HeLa cells were characterised in a time-course study using scanning electron microscopy, confocal microscopy and microarray-based analysis of the HeLa cell transcriptome. At 4 h post infection, cytoadherence of M. hominis to the HeLa cell surface was accompanied by differential regulation of 723 host genes (>2 fold change in expression). Genes associated with immune responses and signal transduction pathways were mainly affected and components involved in cell-cycle regulation, growth and death were highly upregulated. At 48 h post infection, when mycoplasma invasion started, 1588 host genes were differentially expressed and expression of genes for lysosome-specific proteins associated with bacterial lysis was detected. In a chronically infected HeLa cell line (2 weeks), the proportion of intracellular mycoplasmas reached a maximum of 10% and M. hominis-filled protrusions of the host cell membrane were seen by confocal microscopy, suggesting exocytotic dissemination. Of the 1972 regulated host genes, components of the ECM-receptor interaction pathway and phagosome-related integrins were markedly increased. The immune response was quite different to that at the beginning of infection, with a prominent induction of IL1B gene expression, affecting pathways of MAPK signalling, and genes connected with cytokine-cytokine interactions and apoptosis. These data show for the first time the complex, time-dependent reaction of the host directed at mycoplasmal clearance and the counter measures of this pestering pathogen.
人型支原体是一种兼性人类病原体,主要与细菌性阴道病和盆腔炎有关,但它也能够传播到其他部位,导致关节炎,或在新生儿中导致脑膜炎。人型支原体有 537 个注释基因,是自我复制能力最小的支原体之一,因此是研究病原体对宿主的影响的理想模型生物。使用扫描电子显微镜、共聚焦显微镜和基于微阵列的 HeLa 细胞转录组分析,在时间进程研究中,对人型支原体对 HeLa 细胞的黏附、定植和侵袭进行了研究。在感染后 4 小时,人型支原体与人 HeLa 细胞表面的细胞黏附伴随着 723 个宿主基因的差异表达(表达水平变化超过 2 倍)。主要受影响的是与免疫反应和信号转导途径相关的基因,而与细胞周期调控、生长和死亡相关的基因则高度上调。在感染后 48 小时,当支原体开始入侵时,有 1588 个宿主基因差异表达,并且检测到与细菌裂解相关的溶酶体特异性蛋白的基因表达。在慢性感染的 HeLa 细胞系(2 周)中,细胞内支原体的比例达到最大值 10%,并且可以通过共聚焦显微镜观察到充满人型支原体的宿主细胞膜突起,表明发生了胞吐传播。在 1972 个受调控的宿主基因中,细胞外基质受体相互作用途径和吞噬体相关整合素的成分显著增加。与感染初期相比,免疫反应明显不同,白细胞介素 1B 基因的表达明显增加,影响 MAPK 信号通路以及与细胞因子-细胞因子相互作用和细胞凋亡相关的基因。这些数据首次显示了宿主对支原体清除的复杂的、时程依赖的反应,以及这种恼人的病原体的对抗措施。