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首页> 外文期刊>Infection and immunity >Interaction of Bartonella henselae with the Murine Macrophage Cell Line J774: Infection and Proinflammatory Response
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Interaction of Bartonella henselae with the Murine Macrophage Cell Line J774: Infection and Proinflammatory Response

机译：汉赛巴尔通体与小鼠巨噬细胞系J774的相互作用：感染和促炎反应。

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Bartonella henselae is the causative agent of cat scratch disease (CSD), a self-limiting condition characterized by a subacute regional lymphadenopathy that may develop into disseminated bartonellosis in immunocompromised subjects. Mice experimentally infected with B. henselaedisplay typical liver and spleen granulomas rich in T cells and macrophages. So far there are no data on the interaction between bartonellae and macrophages. In order to clarify this topic, we investigated the interaction of B. henselae with J774, a mouse macrophage cell line. Analysis of bacterial uptake by functional assays and transmission electron microscopy indicates that bartonellae can enter and survive inside J774. Entry occurred within 30 min postinfection and reached a plateau at 160 min. Infection of J774 was followed by a dose-dependent release of the proinflammatory cytokines tumor necrosis factor alpha, interleukin 1β (IL-1β), and IL-6. Bartonellae persisted intracellularly without loss of viability for at least 8 h, and their number slightly decreased 24 h postinfection. Gamma interferon (IFN-γ) treatment of J774 significantly decreased the number of recoverable bacteria at 8 and 24 h. This enhancement of macrophage bactericidal activity was associated with nitric oxide (NO) release and was prevented by the addition of the competitive inhibitor of NO synthesis NG -monomethyll-arginine. These findings suggest that IFN-γ-mediated activation of macrophages may be important for the clearing ofB. henselae infection and that anti-B. henselae microbicidal activity of IFN-γ-activated macrophages is mediated to a large extent by NO production.
机译：亨通巴尔通体是猫抓痒病（CSD）的病原体，是一种自限性疾病，其特征是亚急性区域淋巴结病，在免疫功能低下的受试者中可能发展成弥漫性巴尔通体病。实验性感染 B的小鼠。 henselae 表现出典型的富含T细胞和巨噬细胞的肝脏和脾肉芽肿。到目前为止，尚无关于通气管和巨噬细胞之间相互作用的数据。为了阐明这一主题，我们研究了 B的相互作用。 henselae 与小鼠巨噬细胞J774系。通过功能测定和透射电子显微镜对细菌摄取的分析表明，巴尔通体可以进入J774并在其中存活。感染在感染后30分钟内发生，并在160分钟达到平稳。感染J774后，剂量依赖性释放促炎细胞因子肿瘤坏死因子α，白介素1β（IL-1β）和IL-6。巴尔通体在细胞内持续生存至少8 h，并且感染后24 h数量略有下降。 γ干扰素（IFN-γ）对J774的处理在8和24小时时显着降低了可恢复细菌的数量。巨噬细胞杀菌活性的增强与一氧化氮（NO）的释放有关，并且可以通过加入竞争性NO合成抑制剂 N G -单甲基精氨酸来阻止。这些发现表明，IFN-γ介导的巨噬细胞活化对于清除em B可能是重要的。 henselae 感染和抗- B。 IFN-γ活化的巨噬细胞的亨氏菌杀菌活性在很大程度上由NO的产生介导。

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