Stromal IFN-γR-Signaling Modulates Goblet Cell Function During Salmonella Typhimurium Infection
Müller, Andreas J.
Hansson, Gunnar C.
- Journal Article
Rights / licenseCreative Commons Attribution 3.0 Unported
Enteropathogenic bacteria are a frequent cause of diarrhea worldwide. The mucosal defenses against infection are not completely understood. We have used the streptomycin mouse model for Salmonella Typhimurium diarrhea to analyze the role of interferon gamma receptor (IFN-γR)-signaling in mucosal defense. IFN-γ is known to contribute to acute S. Typhimurium diarrhea. We have compared the acute mucosal inflammation in IFN-γR-/- mice and wild type animals. IFN-γR-/- mice harbored increased pathogen loads in the mucosal epithelium and the lamina propria. Surprisingly, the epithelium of the IFN-γR-/- mice did not show the dramatic “loss” of mucus-filled goblet cell vacuoles, a hallmark of the wild type mucosal infection. Using bone marrow chimeric mice we established that IFN-γR-signaling in stromal cells (e.g. goblet cells, enterocytes) controlled mucus excretion/vacuole loss by goblet cells. In contrast, IFN-γR-signaling in bone marrow-derived cells (e.g. macrophages, DCs, PMNs) was required for restricting pathogen growth in the gut tissue. Thus IFN-γR-signaling influences different mucosal responses to infection, including not only pathogen restriction in the lamina propria, but, as shown here, also goblet cell function Show more
Journal / seriesPLoS ONE
Pages / Article No.
PublisherPublic Library of Science
Organisational unit03589 - Hardt, Wolf-Dietrich / Hardt, Wolf-Dietrich
132997 - Mechanism of caspase-1 subversion in Salmonella Typhimurium diarrhea (SNF)
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