Human Macrophages Clear the Biovar Microtus Strain of Yersinia pestis More Efficiently Than Murine Macrophages

Discussion Yersinia pestis has evolved from Y. pseudotuberculosis, a foodborne enteropathogenic pathogen responsible for self-limiting intestinal infections (Morelli et al., 2010). Three pathogenic Yersinia bacteria shared a common 70-Kb virulence plasmid that encodes the type three secretion system (T3SS), which can deliver several Yersinia virulence effectors called Yersinia outer membrane proteins (Yops) into the eukaryotic cell cytosol to paralyze host defenses (Cornelis, 2002). Acquiring pPCP1 and pMT1 plasmids has endowed Y. pestis with new virulent factors such as the F1 capsular antigen, the Pla plasminogen activator, and the murine toxin, all of which are critical for this bacterium to be a flea-transmitted lethal pathogen (Prentice and Rahalison, 2007). Massive gene losses have also played very important roles in the evolution of Y. pestis (Chain et al., 2004). Indeed, several newly acquired features contributing to the high pathogenicity and flea-bite transmissibility of Y. pestis have resulted from reductive evolution. For instance, the Inv and YadA adhesins which are needed for enteropathogenic yersiniae colonization the Peyer's patches and mesenteric lymph nodes, are both pseudogenes in Y. pestis (Marra and Isberg, 1997; Parkhill et al., 2001; Heise and Dersch, 2006). Furthermore, with several biosynthesis gene for LPS being inactivated in Y. pestis, LPS in this bacterium lacks the O antigen and switches from a hexa-acylated to tetra-acylated form that ...
Source: Frontiers in cellular and infection microbiology - Category: Microbiology Source Type: research