The clotting of blood, crucial to wound healing, is carried out by cell fragments called platelets. This is the most established function of platelets, but studies in recent years have begun to hint that platelets may have other important roles in our immune system — like fighting infection.
Now, scientists from the University of Calgary, Canada, seem to have observed proof of this in a study published this week in Nature Immunology. Paul Kubes and his team have identified a new surveillance mechanism in the liver of mice involving platelets.
They noticed that platelets, while sailing across the blood stream in the liver of mice, were making frequent short-lived “touch-and-go” interactions with specialized immune cells called Kupffer cells. Kupffer cells are located in the liver and protect us from infection by capturing and eventually killing bacteria that pass by.
It seemed that this touch-and-go mechanism was how platelets were scanning for captured bacteria. “It is like a security guard going from door to door making sure there are no thieves. If there are none the security guard leaves,” explained Kubes via email to this correspondent.
But when platelets encountered a Kupffer cell bound to bacteria, the platelet-Kupffer cell interaction lasted much longer.
The scientists found out that two receptor proteins on the surface of platelets — GpIb, and the GpIIb-GpIIIa complex have an affinity towards a protein (von Willebrand factor (vWF)) found on the surface of Kupffer cells.
The GpIb receptor binds to the vWF long enough to scan for any captured bacteria. If they find nothing, the platelet detaches and continues along the bloodstream in a touch-and-go interaction.
However, when platelets encountered a Kupffer cell with captured bacteria (Bacillus cereus, or MRSA) the second receptor binds to the Kupffer cell resulting in a more sustained interaction eventually leading up to the killing of the bacteria.
How exactly this binding is helping fight infection is still being examined.
But it is clear that this platelet-mediated surveillance mechanism is crucial to the mice because most (80-100 per cent) mutant mice lacking platelets or GpIb receptors died within four hours of infection, whereas more than 90 per cent of wild-type mice survived.
Though this study was performed in mice, Kube says “there is good evidence that human platelets can kill malaria infected red blood cells and in sepsis platelets appear to also be involved so they likely do play a role in immunity.”
These findings raise several important questions regarding the efficiency of drugs like aspirin, which are known platelet inhibitors. “It is unlikely that aspirin will necessarily make you more susceptible to bacteria but if it allows bacteria to survive longer in blood it could help bacteria become more resistant,” said Kubes. “There may be a need to reconsider aspirin use in immunosuppressed patients.”