Adhesion to the host cell surface is sufficient to mediate<i>Listeria monocytogenes</i>entry into epithelial cells

Abstract

The intestinal epithelium is the first physiological barrier breached by the Gram-positive facultative pathogen <i>Listeria monocytogenes</i> during an in vivo infection. <i>Listeria monocytogenes</i> binds to the epithelial host cell receptor E-cadherin, which mediates a physical link between the bacterium and filamentous actin (F-actin). However, the importance of anchoring the bacterium to F-actin through E-cadherin for bacterial invasion has not been tested directly in epithelial cells. Here we demonstrate that depleting αE-catenin, which indirectly links E-cadherin to F-actin, did not decrease <i>L. monocytogenes</i> invasion of epithelial cells in tissue culture. Instead, invasion increased due to increased bacterial adhesion to epithelial monolayers with compromised cell-cell junctions. Furthermore, expression of a mutant E-cadherin lacking the intracellular domain was sufficient for efficient <i>L. monocytogenes</i> invasion of epithelial cells. Importantly, direct biotin-mediated binding of bacteria to surface lipids in the plasma membrane of host epithelial cells was sufficient for uptake. Our results indicate that the only requirement for <i>L. monocytogenes</i> invasion of epithelial cells is adhesion to the host cell surface, and that E-cadherin-mediated coupling of the bacterium to F-actin is not required.