Abstract
The microbiota of the mammalian intestinal tract represents a formidable barrier to colonization by pathogens. To overcome this resistance to colonization, bacterial pathogens use virulence factors to induce intestinal inflammation, which liberates nutrients for selective use by the infecting microbe. Studies of Salmonella enterica serovar Typhimurium (S. Typhimurium) infection in a streptomycin-treated mouse colitis model show how virulence factor-induced inflammation can produce nutrients used selectively by the pathogen. Type III secreted effectors of invading S. Typhimurium induce inflammation in the intestine (epithelial cells and lamina propria macrophages) that causes changes in the composition of the lumen. For example, neutrophils entering the intestine produce superoxide, resulting in production of tetrathionate, which S. Typhimurium in the lumen uses as an electron acceptor for anaerobic respiration. In their recent study, Lopez et al. demonstrate that S. Typhimurium strains that are lysogenized with a phage encoding type III effector SopE induce the host to produce nitric oxide synthetase (iNOS) in the intestine (C. A. Lopez et al., mBio 3:e00143-12, 2012). Nitric oxide is converted to a highly favorable electron acceptor, nitrate. As a result, growth of sopE(+) S. Typhimurium in the intestine lumen is boosted by nitrate respiration. This is a striking example of how acquisition of a virulence factor by horizontal gene transfer can increase the metabolic fitness of a pathogen. Interestingly, survival of the invading bacteria is probably decreased as a result of the SopE-induced immune response, and yet the S. Typhimurium bacteria that multiply in the lumen of the intestine can efficiently disseminate to another host, ensuring success for the pathogen.