Role of internalin proteins in the pathogenesis of Listeria monocytogenes Original paper

What was reviewed?

This review discussed the roles of internalin proteins (InlA, InlB, InlC, InlF, and InlP) in the pathogenesis of Listeria monocytogenes. The focus was on how these proteins facilitate the bacterium’s ability to invade human host cells, traverse anatomical barriers, and spread within tissues. It emphasized the mechanisms through which these internalins interact with various host receptors, influencing bacterial internalization, cell-to-cell spread, and overall virulence.

Who was reviewed?

The review primarily focused on Listeria monocytogenes and its internalin proteins, specifically InlA, InlB, InlC, InlF, and InlP. These proteins interact with host cell receptors to promote infection and enable the bacterium to cross important barriers such as the intestinal, blood-brain, and placental barriers. The study highlighted how these interactions contribute to the spread of Listeria within the host and to the establishment of systemic infection.

What were the most important findings?

The review found that the internalin proteins of Listeria monocytogenes are crucial for the bacterium’s ability to invade and spread within host tissues. InlA and InlB were identified as key players in the initial entry of bacteria into human cells by binding to E-cadherin and the Met receptor, respectively. InlA-mediated entry is particularly important for Listeria to cross the intestinal barrier by inducing transcytosis in goblet cells, which express E-cadherin on their apical surface. InlC and InlP were found to play significant roles in cell-to-cell spread and placental infection by interacting with Tuba and afadin, respectively, to facilitate bacterial movement through host tissues. Additionally, InlF was highlighted for its role in promoting Listeria entry into brain endothelial cells, contributing to the ability of Listeria to breach the blood-brain barrier. These findings underscore the diverse functions of internalins in facilitating infection at multiple sites and highlight the intricate mechanisms by which Listeria navigates host defenses.

What are the greatest implications of this study?

The review has profound implications for understanding how Listeria monocytogenes causes infection and how it evades host immune defenses. By highlighting the role of internalins in crossing key anatomical barriers and spreading within tissues, the study provides insight into the pathogenesis of Listeria, which can lead to severe conditions like meningitis and abortion. This understanding opens up potential therapeutic avenues, including the development of vaccines or drugs that target specific internalin-host receptor interactions, which could prevent bacterial entry and spread. Additionally, the findings contribute to a deeper understanding of the role of cell adhesion molecules in bacterial pathogenesis and host-pathogen interactions, which is critical for designing effective interventions to combat Listeria infections, particularly in vulnerable populations such as pregnant women and the immunocompromised.