ICMI 2015

W.113 The Influence of the Intestinal Microbiota on Salmonella Infection

Wednesday, July 15, 2015
Grand Hall and Gallery, Ground Floor & 1st Floor (Maritim Hotel)
Maria Fernandez , Department of Immunology and Microbiology, Institute of Biomedicine, Sahlgrenska Academy at The University of Gothenburg, Gothenburg, Sweden
Ulf Alexander Wenzel , Department of Immunology and Microbiology, Institute of Biomedicine, Sahlgrenska Academy at The University of Gothenburg, Gothenburg, Sweden
Ulf Yrlid , Department of Immunology and Microbiology, Institute of Biomedicine, Sahlgrenska Academy at The University of Gothenburg, Gothenburg, Sweden
Fredrik Bäckhed , Wallenberg Laboratory and Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy at The University of Gothenburg, Gothenburg, Sweden
Mary Jo Wick , Department of Immunology and Microbiology, Institute of Biomedicine, Sahlgrenska Academy at The University of Gothenburg, Gothenburg, Sweden
The intestine of humans and other mammals harbors a complex community of microorganisms that contribute to host’s homeostasis. However, several questions remain unanswered about their influence on infection. Here we study the importance of the intestinal microbiota in oral Salmonella infection. We show that germfree mice have a higher bacterial burden in mesenteric lymph nodes (MLN) compared to conventional mice. In contrast, bacterial penetration into the lamina propria of the small intestine is unaltered. The recruitment of neutrophils and monocytes is not altered in Salmonella-infected germfree mice. However, infected germ free mice have a greater population of CD11c+MHC-IIhighCD103+CD11b+ dendritic cells.  Germfree mice also show a higher frequency of IFN-γ-producing NK and CD4+ T cells early during infection. Similarly, adult mice treated with antibiotics and orally infected with Salmonella also have greater bacterial burden and frequency of IFN-γ-producing cells in MLN. Overall, the data suggest that the severity of the infection is a consequence of the lack of competition between Salmonella and the microbiota, rather than alterations in the immune system attributed to the absence of commensals from birth in germfree mice.