Infection of endothelial cells by N. meningitidis (blue) induces the massive recruitment of ezrin and adhesion molecules (red), preventing their accumulation at leukocyte (green) contact sites.
Many inflammation-inducing leukocytes pass from the bloodstream to infected tissues through loosened endothelial cell–cell junctions. The endothelial cells form cup-like actin structures that help leukocytes adhere and migrate. But these cups did not form on endothelial cells where extracellular colonies of Neisseria meningitidis grew, the authors found. Leukocytes thus failed to migrate to cell junctions and were easily detached from the surface by flow.
Cups were absent because the bug sequestered away host ezrin and moesin. These actin-binding proteins, which link adhesion molecules in the plasma membrane to the cytoskeleton, were required for cup formation and seem to be in limited quantities. Overexpression of either ezrin or moesin rescued leukocyte migration between infected cells.
The bug uses ezrin, moesin, and cytoskeletal molecules to adhere tightly to host cells in large, stable colonies. The cytoskeletal changes also allow a few of the bacteria to cross the blood–brain barrier via internalization at the apical surface and exocytosis out the other side, thus leading to meningitis.
By usurping the same molecules that the immune cells use, N. meningitidis probably delays its pursuit by neutrophils, the host's first line of defense. No animal model of meningitis exists, however, to test whether this putative delay is a selective advantage for the bacterium.
This mechanism of immune interference may be specific to N. meningitidis. Most other human pathogenic bacteria, such as Listeria or Shigella, are quickly internalized, and thus have no lasting hold on ezrin or moesin. 
