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Listeria monocytogenes  ( Lm ) is an invasive foodborne pathogen that leads to severe central nervous system and maternal-fetal infections.  Lm  ability to actively cross the intestinal barrier is one of its key pathogenic properties.  Lm  crosses the intestinal epithelium upon the interaction of its surface protein internalin (InlA) with its host receptor E-cadherin (Ecad). InlA-Ecad interaction is species-specific, does not occur in wild-type mice, but does in transgenic mice expressing human Ecad and knock-in mice expressing humanized mouse Ecad. To study listeriosis in wild-type mice, InlA has been “murinized” to interact with mouse Ecad. Here, we demonstrate that, unexpectedly, murinized InlA (InlA m ) mediates not only Ecad-dependent internalization, but also N-cadherin-dependent internalization. Consequently, InlA m -expressing  Lm  targets not only goblet cells expressing luminally-accessible Ecad, as does  Lm  in humanized mice, but also targets villous M cells, which express luminally-accessible N-cadherin. This aberrant  Lm  portal of entry results in enhanced innate immune responses and intestinal barrier damage, both of which are not observed in wild-type  Lm -infected humanized mice. Murinization of InlA therefore not only extends the host range of  Lm , but also broadens its receptor repertoire, providing  Lm  with artifactual pathogenic properties. These results challenge the relevance of using InlA m -expressing  Lm  to study human listeriosis and  in vivo  host responses to this human pathogen.

Murinization of Internalin Extends Its Receptor Repertoire, Altering Listeria monocytogenes Cell Tropism and Host Responses