A Multi-Omic View of Host-Pathogen-Commensal Interplay in Salmonella-Mediated Intestinal Infection
Figure 4
Model of host-pathogen-commensal interactions during S. Typhimurium-induced gastroenteritis.
Using a pan-omics approach, we have developed a model of the interplay between the mouse, S. Typhimurium, and the commensal population during gastrointestinal infection. Prior to pathogen introduction, a Barnesiella-dominated commensal population exists in the homeostatic gut. Early in infection, S. Typhimurium proliferates, stimulates an inflammatory response characterized by neutrophil activation, and disrupts this microbial community. As the commensal population profile changes, so do metabolites in the gut that are normally metabolized by the microbial community. Fucosylated glycan content also increases in the Salmonella-infected gut, potentially as part of an immune response or pathogen clearance mechanism. S. Typhimurium senses and responds to fucose availability during gastrointestinal infection, as evidenced by increased expression of fucose utilization proteins. Finally, pathogen clearance from the gut occurs, allowing the gastrointestinal environment to begin to return to pre-infection conditions.