Final answer:
The key mechanisms central to both intracellular adhesion and entry for Listeria are the surface proteins internalins and the virulence factors listeriolysin O and ActA. These factors enable Listeria to invade host cells, escape vacuoles, and use the host's actin cytoskeleton for intracellular movement and cell-to-cell spread.
Step-by-step explanation:
What is central to both intracellular adhesion and entry for listeria? The central mechanisms that facilitate intracellular adhesion and entry of Listeria monocytogenes, the pathogen causing listeriosis, are the virulence factors, primarily internalins and the proteins listeriolysin O (LLO) and ActA.
Internalins such as InlA and InlB are surface proteins that facilitate the invasion of Listeria into nonphagocytic cells, enabling the pathogen to penetrate the intestinal barrier and disseminate via circulatory and lymphatic systems. Moreover, Listeria uses LLO to escape vacuoles and ActA to move using the actin cytoskeleton of the host, facilitating intercellular movement without entering the extracellular environment, thus spreading the infection efficiently from cell to cell.
Adhesion of Listeria to host cells is critical for infection, involving factors that improve pathogen binding to host cell receptors. Listeria exploits the actin cytoskeleton not only for entry but also for intracellular movement, indicating that interactions with host cell actin are crucial for both adhesion and motility, showcasing the central importance of these mechanisms for the pathogen's lifecycle inside the host.