摘要：CXCR3 and its ligands are heavily associated with inflammation and have been implicated in numerous inflammatory diseases. CXCR3 plays an important role in recruiting pro-inflammatory cells, specifically neutrophils, in a model of sterile colitis whereby CXCR3(-/-) mice showed an attenuated course of colitis with markedly reduced host-tissue damage in the inflamed caecum. The role of CXCR3 during infectious colitis, however, is unclear and therefore in this study, we investigated the role of CXCR3 in the regulation of the immune response during acute and chronic gastrointestinal infection, using a murine model of Salmonella enterica serovar Enteritidis. During acute infection with Salmonella, we observed significantly increased Salmonella loading in the caecum and dissemination to the spleen and liver in CXCR3(-/-) mice, but not in Wt counterparts. During chronic infection, increased pathological features of inflammation were noted in the spleen and liver, with significantly increased levels of apoptosis in the liver of CXCR3(-/-) mice, when compared to Wt counterparts. In addition, compromised intestinal IgA levels, CD4(+) helper T cells and neutrophil recruitment were observed in CXCR3(-/-) challenged with Salmonella, when compared to Wt counterparts. Our data suggests that CXCR3 is a key molecule in host intestinal immunity against Salmonellosis via regulating neutrophils chemotaxis.
