title: Yersinia pestis versus Yersinia pseudotuberculosis: effects on host macrophages.
abstract: Yersinia pestis, the causative agent of plague, is proved to be a recently emerged clone from Y. pseudotuberculosis. However, the diseases they cause and their patterns of transmission are very different. People always focus on the genetic changes between Y. pestis and Y. pseudotuberculosis to reveal their pathogenic differences, and little is known about host defence differences to these two Yersinia. In this study, the effects of Y. pestis and Y. pseudotuberculosis on macrophages were analysed. Cell apoptosis showed significant difference after the macrophages were infected by these two strains, and caspase-3 activity also demonstrated a similar tendency. Further, macrophage function activities were evaluated. We found during the early infection of Y. pestis, several basic functions of macrophages, including phagocytosis, secretion of cytokine tumour necrosis factor-α and nitric oxide, macrophage polarity and antigen presenting, were significantly interrupted. In comparison, Y. pseudotuberculosis infection showed lower inhibition on macrophages. Especially, Y. pestis infection might cause macrophage to polarize to M2 macrophages in the early phase, compared with Y. pseudotuberculosis infection, which was different from the common acute infection. These results clearly indicated even in the early stage of infection, different host macrophage defence patterns could help us to understand the obvious virulence differences between Y. pestis and Y. pseudotuberculosis.
authors.affiliation: State Key Laboratory of Pathogen and Biosecurity, National Center for Biomedical Analysis, Army Center for Microbial Detection and Research, Institute of Microbiology and Epidemiology, Beijing, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Bi
authors.forename: X
authors.initials: X
authors.lastname: Wang
authors.forename: Y
authors.initials: Y
authors.lastname: Han
authors.forename: Z
authors.initials: Z
authors.lastname: Guo
authors.forename: R
authors.initials: R
authors.lastname: Yang
mesh_terms: D000818:Animals; D017951:Antigen Presentation; D017209:Apoptosis / Q000276:immunology; D002454:Cell Differentiation / Q000276:immunology; D002478:Cells, Cultured; D049810:Genetic Speciation; D054884:Host-Pathogen Interactions; D006801:Humans; D008264:Macrophages / Q000276:immunology* / Q000382:microbiology; D051379:Mice; D008807:Mice, Inbred BALB C; D010587:Phagocytosis / Q000276:immunology; D010930:Plague / Q000276:immunology* / Q000382:microbiology* / Q000635:transmission; D013045:Species Specificity; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014774:Virulence / Q000276:immunology; D015010:Yersinia pestis / Q000235:genetics / Q000472:pathogenicity*; D015011:Yersinia pseudotuberculosis / Q000235:genetics / Q000472:pathogenicity*
chemical_list: D014409:Tumor Necrosis Factor-alpha