Neisseria gonorrhoeae use their type IV pili (Tfp) to pull on the epithelial cells they are infecting, say Heather Howie, Magdalene So (Oregon Health and Science University, Portland, OR), and colleagues. This pull, perhaps mimicking normal cell attachment signals, activates gene expression that enhances cell survival.
The Tfp had already shown their talents: their retraction pulls the bacteria along on a surface. The Oregon group now show that infection with Tfp-containing bacteria further activates a subset of genes, mostly MAP kinase targets, that are normally activated by Neisseria infection.
A similar set of genes was induced by pulling on magnetic beads that had been coated with pili proteins and stuck to the epithelial cells. This treatment also reduced apoptotic markers.
At 100 pN of force per retraction event, 10 pili per bacteria, and 10–100 bacteria per microcolony, the force at each site on an epithelial cell may reach 104–105 pN. This is in the same range as the force applied to an integrin complex in a ligament. In many cells such forces are needed to generate survival signals, as they indicate to the cell that it is firmly attached to a substrate. Neisseria may be coopting this signal to boost the survival of its host cells in the face of immune reactions that would tend to eliminate the infected cell.