Abstract

CD103+CD11b+ dendritic cells (DC) are the major migratory DC subset in the small intestine lamina propria (siLP) and their survival is dependent on the transcription factor interferon regulatory factor 4 (IRF4). Mice with a DC-specific deletion of irf4 (CD11c-cre.Irf4 mice) have reduced mucosal CD103+CD11b+ DC and altered T cell differentiation to protein antigen. The influence of CD103+CD11b+ DC on oral infection with the gastrointestinal pathogen Salmonella, however, is poorly understood and is investigated here. We show that, despite being infected with Salmonella, CD11c-cre.Irf4 mice (called Cre+ mice) conserve the reduction in CD103+CD11b+ DC observed in naive Cre+ mice, particularly in the mesenteric lymph nodes (MLN) but also in the siLP at day 3 post infection. Moreover, Salmonella-infected Cre+ mice have a similar bacterial burden in intestinal tissues (siLP, MLN and Peyer’s patches) as well as the spleen compared to infected Cre− controls. The T cell compartment, including the frequency of IFN-γ and IL-17-producing T cells, is not altered in intestinal tissues of Salmonella-infected Cre+ mice relative to infected Cre− controls. In addition, no difference between infected Cre+ and Cre− mice was observed in either the concentration of IL-6 or IL-17 in whole tissue lysates of siLP, MLN or Peyer’s patches or in the serum concentration of Salmonella-specific IgG and IgM. Overall the data suggest that the reduction of CD103+CD11b+ DC in Cre+ mice has little if any impact on Salmonella burden in infected tissues or eliciting effector functions important in host survival at later stages of the infection.

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