Rasch Janine, Krüger Stefanie, Fontvieille Dominique, Ünal Can M, Michel Rolf, Labrosse Aurélie, Steinert Michael
Institut für Mikrobiologie, Technische Universität Braunschweig, Germany.
UMR CARRTEL, Universite de Savoie-INRA, Le Bourget du Lac, France.
Int J Med Microbiol. 2016 Sep;306(6):443-51. doi: 10.1016/j.ijmm.2016.05.012. Epub 2016 May 25.
Legionella pneumophila, the causative agent of Legionnaireś disease, is naturally found in aquatic habitats. The intracellular life cycle within protozoa pre-adapted the "accidental" human pathogen to also infect human professional phagocytes like alveolar macrophages. Previous studies employing the model organism Caenorhabditis elegans suggest that also nematodes might serve as a natural host for L. pneumophila. Here, we report for the first time from a natural co-habitation of L. pneumophila and environmental nematode species within biofilms of a warm water spring. In addition, we identified the protozoan species Oxytricha bifaria, Stylonychia mytilus, Ciliophrya sp. which have never been described as potential interaction partners of L. pneumophila before. Modeling and dissection of the Legionella-protozoa-nematode interaction revealed that C. elegans ruptures Legionella-infected amoebal cells and by this means incorporate the pathogen. Further infection studies revealed that the macrophage infectivity potentiator (Mip) protein of L. pneumophila, which is known to bind collagen IV during human lung infection, promotes the colonization of the intestinal tract of L4 larvae of C. elegans and negatively influences the life span of the worms. The Mip-negative L. pneumophila mutant exhibited a 32-fold reduced colonization rate of the nematodes after 48h when compared to the wild-type strain. Taken together, these studies suggest that nematodes may serve as natural hosts for L. pneumophila, promote their persistence and dissemination in the environment, and co-evolutionarily pre-adapt the pathogen for interactions with extracellular constituents of human lung tissue.
嗜肺军团菌是军团病的病原体,天然存在于水生栖息地。它在原生动物内的细胞内生命周期使这种“偶然的”人类病原体预先适应了感染人类专业吞噬细胞,如肺泡巨噬细胞。此前利用模式生物秀丽隐杆线虫进行的研究表明,线虫也可能是嗜肺军团菌的天然宿主。在此,我们首次报道了嗜肺军团菌与温水泉生物膜内环境线虫物种的自然共存情况。此外,我们鉴定出了双叉尖毛虫、贻贝急游虫、纤毛虫属等原生动物物种,这些物种此前从未被描述为嗜肺军团菌的潜在相互作用伙伴。对军团菌-原生动物-线虫相互作用的建模和剖析显示,秀丽隐杆线虫会破坏被军团菌感染的变形虫细胞,并借此摄取病原体。进一步的感染研究表明,嗜肺军团菌的巨噬细胞感染增强蛋白(Mip)在人类肺部感染期间已知会结合IV型胶原蛋白,它能促进嗜肺军团菌在秀丽隐杆线虫L4幼虫肠道内的定殖,并对蠕虫的寿命产生负面影响。与野生型菌株相比,Mip阴性的嗜肺军团菌突变体在48小时后对线虫的定殖率降低了32倍。综上所述,这些研究表明线虫可能是嗜肺军团菌的天然宿主,促进其在环境中的持久性和传播,并在共同进化过程中使病原体预先适应与人类肺组织细胞外成分的相互作用。