1939, reveals that invading Neisseria meningitidis bacteria must rely on pauses in blood flow in order to attach to the edge of blood vessels.
Colonization of the nose and throat by N. meningitidis bacteria is not uncommon in the general population. If these bacteria gain access to the bloodstream, however, they can cause septicemia and may even cross the blood–brain barrier to cause meningitis.
In brain samples from a meningococcal sepsis victim, Mairey et al. found that N. meningitidis were not distributed evenly throughout the blood vessels but were instead specifically restricted to capillaries. Since blood flow in capillaries of the brain has been reported to be very hetereogenous, their finding suggested that flow rate, or shear stress, might influence bacterial adhesion. Mairey and colleagues examined blood flow in the brain of live rats and found, to their amazement, that in some capillaries blood flow transiently slows and sometimes even stops.
In vitro, N. meningitidis bound readily to human endothelial cells under low-flow conditions but much less readily during faster flow. Once bound, the bacteria remained steadfastly attached even when the flow speed was subsequently increased. This slow-to-fast transition in flow rate essentially mimicked the changes in blood flow observed in the live rat brain, and the authors suggest that transient slowing of blood in the human brain provides N. meningitidis with the opportunity to bind to and subsequently breach the blood–brain barrier.
“It is not clear whether this [change in flow speed] happens more or less frequently in brain compared to other organs” says Guillaume Dumenil, who led the research. Indeed the team found N. meningitidis in capillaries of other organs. In the brain, however, there is evidence that astrocytes can cause the endothelial cells of arterioles to contract, thus reducing vessel diameter and potentially causing a temporary reduction in blood flow.