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We established a newBrucella neotomae in vitro model system for study of type IV secretion system-dependent (T4SS) pathogenesis in theBrucella genus. Importantly,B. neotomae is a rodent pathogen, and unlikeB. abortus ,B. melitensis , andB. suis ,B. neotomae has not been observed to infect humans. It therefore can be handled more facilely using biosafety level 2 practices. More particularly, using a series of novel fluorescent protein andlux operon reporter systems to differentially label pathogens and track intracellular replication, we confirmed T4SS-dependent intracellular growth ofB. neotomae in macrophage cell lines. Furthermore,B. neotomae exhibited early endosomal (LAMP-1) and late endoplasmic reticulum (calreticulin)-associated phagosome maturation. These findings recapitulate prior observations for human-pathogenicBrucella spp. In addition, during coinfection experiments withLegionella pneumophila , we found that defective intracellular replication of aB. neotomae T4SSvirB4 mutant was rescued and baseline levels of intracellular replication of wild-typeB. neotomae were significantly stimulated by coinfection with wild-type but not T4SS mutantL. pneumophila . Using confocal microscopy, it was determined that intracellular colocalization ofB. neotomae andL. pneumophila was required for rescue and that colocalization came at a cost toL. pneumophila fitness. These findings were not completely expected based on known temporal and qualitative differences in the intracellular life cycles of these two pathogens. Taken together, we have developed a new system for studyingin vitro Brucella pathogenesis and found a remarkable T4SS-dependent interplay betweenBrucella andLegionella during macrophage coinfection.

Promotion and Rescue of Intracellular Brucella neotomae Replication during Coinfection with Legionella pneumophila