Pathogenic enterobacteria face various oxygen (O 2 ) levels during intestinal colonization from the O 2 -deprived lumen to oxygenated tissues. Using Shigella flexneri as a model, we had previously demonstrated that epithelium invasion is promoted by O 2 in a Type III secretion system (T3SS)dependent manner 1 . However, subsequent pathogen adaptation to tissue oxygenation modulation remained unknown. Assessing single-cell distribution, together with tissue oxygenation, we demonstrate here that the colonic mucosa O 2 is actively depleted by Shigella flexneri aerobic respiration, not host neutrophils, during infection, leading to the formation of hypoxic foci of infection. This process is promoted by T3SS inactivation in infected tissues, favoring colonizers over explorers. We identify the molecular mechanisms supporting infectious hypoxia induction, Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:

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