Neisseria gonorrhoeae, Haemophilus influenzae and a handful of other Gram-negative pathogens cling to and invade human cells by co-opting a family of human host cell adhesion molecules called CEACAMs (carcinoembryonic antigen–related cell adhesion molecules). Humans have evolved a counterstrategy: phagocytic cells express CEACAMs, which enable them to efficiently mop up the bacteria (human granulocyte shown here, shoveling in N. gonorrhoeae).

Credit: Reprinted with permission from Rockefeller University Press

In the 5 January Journal of Experimental Medicine, Tim Schmitter et al. identify CEACAM3 as the main mediator during granulocyte uptake, and show that CEACAM3 operates via the small GTPase Rac. The authors found that blocking CEACAM3 or interfering with Rac stimulation reduced phagocyte clearance of N. gonorrhoeae and other CEACAM-binding bacteria. These bacteria do not infect nonhuman primates or rodents, but they regularly colonize mucosal surfaces in people. When the normally benign balance between bacterial invasion and bacterial clearance tilts, the microbes become dangerous.