Abstract

Abstract Foodborne Listeria monocytogenes (LM) causes serious illness & death every year in the US. Ingestion of LM can lead to septicemia, meningitis, & abortion. IL17 is secreted by T cells and regulates the production of CXC chemokines for monocyte and neutrophil recruitment to infected tissue. Foodborne LM infection occurs through the oral route, but mice are highly resistant to oral infection. Here, using a murinized LM strain, we explored the role of IL17RA signaling following oral LM infection. Mortality & body weight loss were compared after LM infection of C57BL/6 & IL17RA-KO mice. LM-specific proliferative responses of splenocytes isolated from infected mice were performed. Viable LM from liver & spleen tissue were enumerated. Neutrophil infiltration & inflammation were evaluated histologically. RT-PCR arrays were used to quantitate cytokine/chemokine mRNA expression in infected tissues. IL17RA-KO mice lost more body weight and died earlier following oral infection than infected WT mice. LM-Ag treated splenocytes from KO mice proliferated less vigorously than WT splenocytes. Tissues from infected IL17RA-KO mice had lower mRNA expression for IFN-γ, IL1-β & iNOS. Liver, spleen & gastric tissues from infected IL17RAKO mice showed increased necrotic tissue damage & increased LM burden. These results indicate that IL17RA signaling is important in host resistance to oral LM infection.

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