Figure 3. Pathogen overcome commensal-mediated resistance through multiple strategies.

a| Pathogenic Escherichia coli: Pathogenic E. coli is capable of utilizing carbohydrates and other resources, such as ethanolamine distinct from that scavenged by commensals. Pathogenic E. coli can also localize to the intestinal epithelial surface that is devoid of commensal microbiota through expression of adhesion molecules, such as intimin. Pathogen-induced gut inflammation confers a growth advantage to the pathogen through the generation of molecules such as inducible nitric oxide synthase (iNOS) expression by host innate immune cells leading to the release of nitrate (NO₃-) that can be utilized as an electron acceptor by E. coli to generate energy through nitrate respiration. Commensal obligate anaerobes, such as Bacteroidetes or Firmicutes lack this ability.

b| Salmonella spp.: Lipocalin-2 derived from host cells block commensal bacterial iron uptake by binding to the bacterial siderophore, enterobactin. Salmonella, however, has a distinct siderophore, salmochelin, for iron uptake, which is not blocked by lipocalin-2. Salmonella-induced gut inflammation also promotes migration of neutrophils that produce reactive oxygen species (ROS), which facilitate conversion of thiosulphate (S₂O₃^2-), generated by commensal bacteria, into tetrathionate (S₄O₆^2-). Salmonella, but not commensals, is capable of utilizing tetrathionate as an electron acceptor for anaerobic respiration.