Figure 1.

Iron acquisition of S. enterica serotype Typhimurium (Salmonella) in the inflamed intestine. S. enterica serotype Typhimurium triggers intestinal inflammation by invading epithelial cells and surviving in mononuclear phagocytes (i.e., macrophages and dendritic cells). The resulting production of IL-22 triggers the production of epithelial derived lipocalin-2. Lipocalin-2 prevents bacterial iron acquisition by binding the siderophore enterochelin, which is produced by both S. enterica serotype typhimurium and commensal E. coli. By producing salmochelin, a siderophore not bound by lipocalin-2, S. enterica serotype Typhimurium can benefit from antimicrobial responses encountered in the intestinal lumen by outgrowing competing intestinal microbes.