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The Gut Microbiota Reduces Colonization of the Mesenteric Lymph Nodes and IL-12-Independent IFN-gamma Production During Salmonella Infection

Journal article
Authors Maria Fernández-Santoscoy
Ulf Alexander Wenzel
Ulf Yrlid
Susanna Cardell
Fredrik Bäckhed
Mary Jo Wick
Published in Frontiers in Cellular and Infection Microbiology
Volume 5
ISSN 2235-2988
Publication year 2015
Published at Wallenberg Laboratory
Institute of Biomedicine, Department of Microbiology and Immunology
Institute of Medicine, Department of Molecular and Clinical Medicine
Language en
Links dx.doi.org/10.3389/fcimb.2015.00093
Keywords Salmonella, microbiota, germ-free mice, infection, IFN-gamma production, intestinal immune-responses, commensal microbiota, antimicrobial, peptides, paneth cells, host, bacteria, typhimurium, innate, system, inflammation, Immunology, Microbiology
Subject categories Microbiology in the medical area, Immunology in the medical area

Abstract

The intestinal commensal microbiota is essential for many host physiological processes, but its impact on infectious diseases is poorly understood. Here we investigate the influence of the gut microbiota during oral Salmonella infection. We report a higher bacterial burden in mesenteric lymph nodes (MLN) of intragastrically infected germ-free (GF) mice compared to conventionally-raised (CONV-R) animals, despite similar inflammatory phagocyte recruitment. Salmonella penetration into the lamina propria of the small intestine and splenic bacterial burden were not altered in the absence of the microbiota. Intragastrically infected GF mice also displayed a higher frequency of IFN-gamma-producing NK, NKT, CD4(+), and CD8(+) T cells in the MLN despite IL-12 levels similar to infected CONV-R mice. However, infecting mice intraperitoneally abrogated the difference in MLN bacterial load and IFN-gamma-producing cells observed in intragastrically-infected animals. Moreover, mice treated with antibiotics (ABX) and intragastrically infected with Salmonella had a greater bacterial burden and frequency of IFN-gamma-producing cells in the MLN. In ABX mice the number of Salmonella correlated with the frequency of IFN-gamma-producing lymphocytes in the MLN, while no such correlation was observed in the MLN of infected GF mice. Overall, the data show that the lack of the microbiota influences pathogen colonization of the MLN, and the increased IFN-gamma in the MLN of infected GF mice is not only due to the absence of commensals at the time of infection but the lack of immune signals provided by the microbiota from birth.

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