Abstract
Abstract Salmonella spp. is responsible for the vast majority of foodborne illnesses in the US. Adenosine is an antiinflammatory mediator that limits tissue damage during inflammation. Surface enzymes CD39 & CD73 mediate the synthesis of extracellular adenosine & can regulate immune responses. We studied the expression of CD39 & CD73 in liver & spleen after infection of C57BL/6 mice with Salmonella enterica serotype Typhimurium (ST) & evaluated the role of CD73 after oral infection of wildtype & CD73-KO mice, in regulating immune responses & bacterial persistence. Liver & spleen cytokine mRNA expression was tested by RT-PCR. Cytokines were assayed by ELISA from cultured supernatant of activated splenocytes. Splenocyte-derived Th cells were tested for intracellular cytokines by FACS. Inflammatory responses in infected CD73-/- mouse livers were tested in H&E sections. Bacterial count was done from liver tissues. After ST infection of wildtype mice, both CD39 & CD73 transcript levels declined in spleen & liver. Splenocytes from ST-infected CD73-/- mice produced significantly more IFN-γ & IL17a. Infected CD73-/- mice had higher expressions of IFN-γ & TNF-α mRNA in liver. Histological examinations of liver sections showed significantly greater number of “inflammatory-foci”. Liver bacterial load was significantly lower in CD73-/-mice. CD73 expression contributes to adenosine accumulation that attenuates inflammation during Salmonellosis & may impair immunity to favor bacterial persistence.
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