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Citrobacter rodentium  is an intestinal mouse pathogen widely used as a model to study the mucosal response to infection. Inbred mouse strains suffer one of two fates following infection: self-limiting colitis or fatal diarrheal disease. We previously reported that  Rspo2  is a major genetic determinant of the outcome of  C .  rodentium  infection;  Rspo2  induction during infection of susceptible mice leads to loss of intestinal function and mortality.  Rspo2  induction does not impact bacterial colonization, but rather, impedes the ability of the host to tolerate  C .  rodentium  infection. Here, we performed deep RNA sequencing and systematically analyzed the global gene expression profiles of  C .  rodentium -infected colon tissues from susceptible and resistant congenic mice strains to determine the common responses to infection and the  Rspo2 -mediated dysfunction pathway signatures associated with loss of disease tolerance. Our results highlight changes in metabolism, tissue remodeling, and host defence as common responses to infection. Conversely, increased Wnt and stem cell signatures, loss of epithelial differentiation, and exaggerated CD4 +  T cell activation through increased antigen processing and presentation were specifically associated with the response to infection in susceptible mice. These data provide insights into the molecular mechanisms underlying intestinal dysfunction and disease tolerance during  C .  rodentium  infection.

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Loss of disease tolerance during Citrobacter rodentium infection is associated with impaired epithelial differentiation and hyperactivation of T cell responses