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- W2761034260 abstract "The enteropathogenic yersiniae normally cause self-limiting gut-associated disease. However, severe secondary disease (e.g. reactive arthritis) can appear after primary infection. In the past, some clinical data suggested that the development of secondary disease is connected with Yersinia persistence. Up to date, only little is known about the influence of Yersinia virulence factors on the pathogenesis of persistent Y. pseudotuberculosis infections.Two sequenced Y. pseudotuberculosis isolates encode the cytotoxic necrotizing factor (CNFY) toxin. The CNFY is important for Y. pseudotuberculosis virulence, as it modulates inflammation and immune responses by enhancing the translocation of Yersinia effector proteins into host cells. Moreover, deletion of CNFY elicits asymptomatic colonization of the gut tissues.In this study, it is shown that CNFY decreased Y. pseudotuberculosis persistence in the mouse model. Impaired persistence of CNFY+ Y. pseudotuberculosis was connected with increased inflammation, severe diarrhea and dysbiosis during acute infection. In contrast, persistent Yersinia infections triggered little inflammation. In addition, the engineering of stable fluorescent Y. pseudotuberculosis enabled the detection of re-organized bacterial colonization patterns from acute to persistent infection, which encompassed formation of dense bacterial aggregates and the absence of microcolonies. The assessment of the host transcriptome and cytokine levels in the cecum during acute Y. pseudotuberculosis infection revealed that CNFY modulated the cecal cytokine and transcriptional landscape, which seemed to further either bacterial clearance or bacterial persistence. During persistent Yersinia infection, it appeared that yersiniae triggered a limited immune response. The characterization of important Y. pseudotuberculosis virulence and persistence genes during acute and persistent infection demonstrated that the CNFY-dependent inflammatory milieu modulated bacterial transcriptional adaptation during the infection. Additionally, this study showed that CNFY increased early bacterial dissemination to systemic tissues, which was dependent on the inflammasome and IL-1 cytokines.In summary, this work provides evidence, that CNFY is a crucial regulator of Y. pseudotuberculosis pathogenesis." @default.
- W2761034260 created "2017-10-20" @default.
- W2761034260 creator A5079271446 @default.
- W2761034260 date "2017-07-06" @default.
- W2761034260 modified "2023-09-26" @default.
- W2761034260 title "The influence of the cytotoxic necrotizing factor toxin of Yersinia pseudotuberculosis on pathogenesis" @default.
- W2761034260 doi "https://doi.org/10.24355/dbbs.084-201707060942" @default.
- W2761034260 hasPublicationYear "2017" @default.
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