In their study, the researchers performed flow chamber experiments under controlled shear stress to examine real-time interactions between the bacterium and endothelium. They also used particle tracking methods to examine the interactions in blood vessels of live mice. In the flow chamber system, the researchers tagged the B. burgdorferi
bacterium with a fluorescent marker, in order to use a microscope to more easily follow its movement along the vessel.
Their experiments showed that the bacterium not only uses the bacterial protein BBK32 to form catch bonds with the endothelium, but also that it uses tethers to stabilize and strengthen these bonds. They found that the bacteria can travel along the endothelium without detaching, by transferring mechanical force from one catch bond to the next, as these bonds are successively formed and broken; the bacteria slowed down whenever they formed a new bond with the endothelium, and then accelerated as they broke a bond and moved on to form a new one.
The researchers also showed that the force produced by bacterial motility (by virtue of bacterial flagella) was greater than the force that blood flow placed on bonds between the bacteria and endothelium during most interactions. This suggests that the bacteria can overcome the force of the blood flow, using their flagella to control where they leave a blood vessel to infect certain tissues.
Overall, these studies show that B. burgdorferi
interacts with endothelial surfaces in a similar way to how leukocytes interact with endothelial surfaces. “We propose that catch bonds and tethering are common cellular responses to the universal problem of vascular adhesion under shear stress, and likely facilitate dissemination of other extracellular pathogens,” the authors conclude.
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