We hypothesize that this may be a consequence of the increased expression of virulence machineries, such as the T3SS, in the ∆croI strain which leads to an increase in damage to the epithelial cell barrier, and an increase in translocation of bacteria entering host circulation.22,36,37 Analysis of the tissue-derived cytokine profile across the large intestine did not identify any major changes between WT- and ∆croI-infected tissues, although there was a trend toward decreased levels of cecal TNFα in the context of ∆croI infection (Figure S5A-B). This evidence concerns the gene TNF and infection.