Infection often leads to inflammatory immune responses; no surprises there. It has long been speculated, however, that the ability to induce intestinal inflammatory responses favours pathogen growth. Most hypotheses on how this might occur have centred on nutrient release through tissue damage or on the intestinal epithelial cells secreting macromolecules, such as extracellular matrix proteins, that can be used as nutrient sources. But the underlying molecular mechanisms of inflammation-induced nutrient availability for pathogens have remained largely elusive. In a remarkable paper on page 426 of this issue, Winter et al. connect the production by the mammalian host of reactive oxygen species — as part of the inflammatory response to the pathogenic bacterium Salmonella enterica serotype Typhimurium — to a unique, metabolic pathway in the pathogen that allows it to compete with the resident gut microbiota.
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