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Santos RL et al. – Initial responses generated by bacterial host cell interaction are amplified in tissue through the interleukin (IL)–18/interferon–gamma and IL–23/IL–17 axes, resulting in the activation of mucosal barrier functions against NTS dissemination. However, the pathogen is adapted to survive antimicrobial defenses encountered in the lumen of the inflamed intestine. This strategy enables NTS to exploit inflammation to outcompete the intestinal microbiota, and promotes the Salmonella transmission by the fecal/oral route.

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