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In the 1980s, seminal scientific research demonstrated that the role of platelets is not limited to blood clotting. The work showed how platelets can also kill some parasites. This other function of platelets was realized when scientists observed the presence of certain receptors, called IgE receptors, on the surface of platelets. IgE receptors are antibodies whose main function is to fight parasitic infections.
Also in the 1980s, other scientists observed that platelets appeared depleted in rabbits suffering airway constriction due to allergies. These observations were the initial findings that helped confirm that platelets have a broader role than their role in blood flow and clotting.. It is now clear that platelets play a direct role in allergic reactions. Specifically, they impact other cells of the immune system during inflammatory reactions to help recruit leukocytes into tissues. Not only do their coordinate inflammation responses, but they are also activated by other inflammatory mediators. When platelets are depleted, leukocytes are not as populous within tissues as when platelets are present in normal amounts.
Because of their specific role in inflammation, platelets are critical in inflammatory diseases other than allergies, such as asthma. Research in both animals and humans has demonstrated that platelets are also associated with the pathogenesis of aspirin-exacerbated respiratory disease (AERD), which is an inflammatory disease that involves not only asthma but also nasal polyposis and pathognomonic respiratory reactions when aspirin is ingested.
When asthma occurs, changes in platelet activity are often observed, including changes in the amount of platelet secretion, as well as the molecules that are expressed on the surface of platelets. Asthma and allergies are also associated with abnormalities of both the aggregation and adhesion of platelets to one another.
In this scenario, platelets have been referred to as “exhausted platelets” that may have been activated too often during allergic responses and are thus unable to respond appropriately when needed for clotting functions. Accordingly, people with allergic disease often have what is referred to as a mild hemostatic defect, where it takes them longer to stop bleeding when they are cut than those without allergies. On the flip side, this group of people may also experience cardiovascular benefits as a result of their reduced clotting. Some research has suggested that these people have less calcified arteries.
The specific activities of platelets within the immune system lead to the pathogenesis of asthma in a few different ways. First, platelets cause bronchoconstriction. They do this by releasing what is known as spasmogens, which included chemicals like serotonin. Second, they lead to the remodeling of the walls of the airway by signaling to a number of relevant cells to modify their activities. Third, they cause inflammation of the airway, which is often accompanied by the release of free radicals. Free radicals are physiologically destructive and often associated with poor health.
The blood-related effects that are seen in patients with allergy and asthma are likely a result of reduced platelet survival time, which can be reversed with glucocorticosteroid medications. However, given that platelet activity can both help and harm people, depending on the context in which the platelets are activated, as well as on the specific needs of the person, it is important not to aim to minimize or maximize platelet activity but instead to find a balance that optimizes outcomes. As more research helps clarify the specific role of platelets in allergies and asthma, new treatments options that involve platelet activity will likely be developed.