Functional Similarities between theicm/dotPathogenesis Systems ofCoxiella burnetiiandLegionella pneumophila

Publisher Website
Google Scholar
Abstract
Coxiella burnetii, the etiological agent of Q fever, is an obligate intracellular pathogen, whereasLegionella pneumophila, the causative agent of Legionnaires' disease, is a facultative intracellular pathogen. During infection of humans both of these pathogens multiply in alveolar macrophages inside a closed phagosome.L. pneumophilaintracellular multiplication was shown to be dependent on theicm/dotsystem, which probably encodes a type IV-related translocation apparatus. Recently, genes homologous to all of theL. pneumophila icm/dotgenes (besidesicmR) were found inC. burnetii.To explore the similarities and differences between theicm/dotpathogenesis systems of these two pathogens, interspecies complementation analysis was performed. NineC. burnetii icmhomologous genes (icmT,icmS,icmQ,icmP,icmO,icmJ,icmB,icmW, andicmX) were cloned under regulation of the correspondingL. pneumophila icmgenes and examined for the ability to complementL. pneumophilamutants with mutations in these genes. TheC. burnetii icmSandicmWhomologous genes were found to complement the correspondingL. pneumophila icmmutants to wild-type levels of intracellular growth in both HL-60-derived human macrophages andAcanthamoeba castellanii. In addition, theC. burnetii icmThomologous gene was found to completely complement anL. pneumophilainsertion mutant for intracellular growth in HL-60-derived human macrophages, but it only partially complemented the same mutant for intracellular growth inA. castellanii. Moreover, as previously shown forL. pneumophila, the proteins encoded by theC. burnetii icmSandicmWhomologous genes were found to interact with one another, and interspecies protein interaction was observed as well. Our results strongly indicate that the Icm/Dot pathogenesis systems ofC. burnetiiandL. pneumophilahave common features.