作者: Bárbara M. Schultz , Geraldyne A. Salazar , Carolina A. Paduro , Catalina Pardo-Roa , Daniela P. Pizarro
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摘要: Chronic intestinal inflammations are triggered by genetic and environmental components. However, it remains unclear how specific changes in the microbiota, host immunity, or pathogen exposure could promote onset exacerbation of these diseases. Here, we evaluated whether Salmonella enterica serovar Typhimurium (S. Typhimurium) infection increases susceptibility to develop inflammation mice. Two mouse models were used evaluate impact S. infection: chemical induction colitis dextran sulfate sodium (DSS) interleukin (IL)-10-/- mice, which spontaneous inflammation. We observed that makes DSS-treated IL-10-/- mice more susceptible Importantly, this increased is associated ability persist liver spleen infected depends on virulence proteins secreted Pathogenicity Island 2-encoded type three secretion system (TTSS-2). Although immunization with a live attenuated vaccine resulted moderate reduction due previous infection, did not prevent bacterial persistence. Our results suggest persistent may increase intestine, be TTSS-2.