Revisited model of InlA^m-expressing bacteria at the intestinal epithelium.

<p>In humanized mEcad-expressing E16P mouse, as well as in human, <i>Lm</i> targets accessible Ecad around intestinal goblet cells to cross intestinal epithelium, without inducing significant intestinal response. The wt InlA of <i>Lm</i> does not interact with mEcad, thus limits the ability of <i>Lm</i> to cross wt mouse intestinal epithelium. Murinization of InlA enables <i>Lm</i>-<i>inlA^m</i> to interact with mEcad and also Ncad of mouse. <i>Lm-inlA^m</i> therefore invades not only the goblet cells but also the villous M cells expressing accessible Ncad in the intestinal epithelia of mice. Targeting of villous M cells, which is not observed in <i>Lm</i>-infected E16P KI mice and is not predicted to occur in humans, results in severe intestinal inflammation which induces polymorphonuclear neutrophil (PMN) infiltration, intestinal barrier damage and a delayed systemic dissemination in wt mice, all of which are not observed in human listeriosis and <i>Lm</i>-infected humanized mice.