I have often suspected it, but we now have fresh evidence that blood platelets have a role in the immune system as well as in thrombosis.
Freom the New Scientist:
When bacteria enter blood they rapidly become coated in platelets, says Dirk Busch at the University of Munich in Germany. These sticky cell fragments then direct bacteria to the spleen, where they are engulfed by dendritic cells – immune cells that trigger a full-blown immune response.
This process relies on the interaction between a platelet receptor called GPIb and a blood protein called C3, which sticks to bacteria. When mice bred to lack C3 were injected with Listeria monocytogenes, platelets failed to surround the bacteria. Instead, they were destroyed by a different immune cell, the macrophage.
Although the macrophages cleared the bacteria, the lack of C3 prevented the formation of immunological memory – which enables the immune system to remember foreign invaders and respond to a future attack. Ultimately, Busch says it might be possible to boost platelet response to improve vaccines.
4 comments:
There are various compounds used as anti-coagulants (aspirin, warfarin, pradaxa, low molecular weight heparin etc) and I am wondering if these might reduce the ability of the platelets to attach to bacteria. Perhaps they all act on pathways different than the one you mentioned.
Regards, TomD
Aspirin certainly does, but recent evidence suggests that aspirin reduces the risk of colon cancer in people who are genetically predisposed to it. These interactions are very complex.
Your last comment was intrigueing. My family history suggests that the possibility of an inherited CRC syndrome may be increased.
Am I understanding correctly that continued prophylactic asprin may further reduce immunity response to vaccination but may reduce CRC developing as a spin off. Does this also apply to the antiplatelet dipyridamole?
probably
Post a Comment