Role of internalin proteins in the pathogenesis of Listeria monocytogenes

Listeria monocytogenes is a food-borne bacterium that causes gastroenteritis, meningitis, or abortion. L. monocytogenes induces its internalization (entry) into human cells and either spreads laterally in tissues or transcytoses to traverse anatomical barriers. In this review, we discuss mechanisms by which five structurally related proteins of the internalin family of L. monocytogenes (InlA, InlB, InlC, InlF, and InlP) interact with distinct host receptors to promote infection of human cells and/or crossing of the intestinal, blood-brain, or placental barriers. We focus on recent results demonstrating that the internalin proteins InlA, InlB, and InlC exploit exocytic pathways to stimulate transcytosis, entry, or cell-to-cell spread, respectively. We also discuss evidence that InlA-mediated transcytosis contributes to traversal of the intestinal barrier, whereas InlF promotes entry into endothelial cells to breach the blood-brain barrier. InlB also facilitates the crossing of the blood-brain barrier, but does so by extending the longevity of infected monocytes that may subsequently act as a Trojan horse to transfer bacteria to the brain. InlA, InlB, and InlP each contribute to fetoplacental infection by targeting syncytiotrophoblast or cytotrophoblast layers of the placenta. This work highlights the diverse functions of internalins and the complex mechanisms by which these structurally related proteins contribute to disease.

Automated summary

The review explores the mechanisms by which Listeria monocytogenes interacts with host receptors through inner proteins, facilitating infection and traversal of anatomical barriers. It highlights the diverse functions of internalins and their complex contribution to disease development.