Multiple distinct types of intracellular bacterial pathogens have been shown to alter the mechanics of their mammalian host cells to promote their spread. Conversely, host cells may respond by altering their own mechanical behavior to limit infection. We have monitored epithelial cell monolayers sparsely infected with the intracellular bacterial pathogen Listeria monocytogenes over the course of several days. As the bacteria replicate and spread from cell to cell, the infected host cells become softer and exert less traction on their extracellular matrix. Uninfected cells surrounding the infection focus become stiffer and actively move toward the site of infection, collectively squeezing the infected cells up into an extruding mound at late times post-infection. Bacteria in mounds are less able to spread laterally in the monolayer, limiting the growth of the focus, while mounded cells eventually undergo death. The cellular competition between infected and uninfected cells leading to mound formation is driven by active directional migration in surrounding uninfected cells, intact cell-cell junctions and innate immune signaling. Our results underline the dynamic remodeling capability of epithelial tissue and propose a general cooperative epithelial extrusion mechanism that could help to limit the local spread of infection.### Competing Interest StatementThe authors have declared no competing interest.

Mechanical competition triggered by innate immune signaling drives the collective extrusion of bacterially-infected epithelial cells