Apical adhesion of meningococci controls host cell basal traction force through Ancreopodia formation

Recent research has unveiled a novel mechanism by which Neisseria meningitidis, a bacterial pathogen, manipulates host cell mechanics during infection. The study, conducted using various in vitro models and advanced imaging techniques, reveals that the bacterium's adhesion to endothelial cells triggers a cascade of mechanical events.

These events culminate in the formation of unique structures known as ancreopodia, which link the bacterial colonies to the basal extracellular matrix. Ancreopodia are actin-rich formations that span the cell thickness, connecting the bacterial colonies to reorganized basal stress fibers and focal-adhesion components. Dynamic imaging studies showed that both the bacterial colonies and mechanosensitive proteins move in a coordinated manner during this process.

Crucially, the analysis of pilus mutants demonstrated that pilus retraction is essential for focusing traction forces beneath the bacterial colonies. Further experiments revealed that disruptions in branched actin assembly or myosin-II activity impair the apico-basal organization and vinculin recruitment, highlighting the critical role of these components in this mechanotransduction process.

The findings of this study have significant implications, as they demonstrate that Nm infection not only enhances local anchoring but also restricts single-cell migration and collective endothelial dynamics. By identifying ancreopodia as a vertical mechanotransduction structure, this research provides valuable insights into the mechanisms through which extracellular pathogens interact with their host cells and reshape host-cell mechanics.