Abstract
Allergic asthma is a chronic and heterogeneous pulmonary disease in which platelets can be activated in an IgE-mediated pathway and migrate to the airways via CCR3-dependent mechanism. Activated platelets secrete IL-33, Dkk-1, and 5-HT or overexpress CD40L on the cell surfaces to induce Type 2 immune response or interact with TSLP-stimulated myeloid DCs through the RANK-RANKL-dependent manner to tune the sensitization stage of allergic asthma. Additionally, platelets can mediate leukocyte infiltration into the lungs through P-selectin-mediated interaction with PSGL-1 and upregulate integrin expression in activated leukocytes. Platelets release myl9/12 protein to recruit CD4+CD69+ T cells to the inflammatory sites. Bronchoactive mediators, enzymes, and ROS released by platelets also contribute to the pathogenesis of allergic asthma. GM-CSF from platelets inhibits the eosinophil apoptosis, thus enhancing the chronic inflammatory response and tissue damage. Functional alterations in the mitochondria of platelets in allergic asthmatic lungs further confirm the role of platelets in the inflammation response. Given the extensive roles of platelets in allergic asthma, antiplatelet drugs have been tested in some allergic asthma patients. Therefore, elucidating the role of platelets in the pathogenesis of allergic asthma will provide us with new insights and lead to novel approaches in the treatment of this disease.
Highlights
Asthma is a chronic and heterogeneous pulmonary disease which affects over 300 million people around the world [1]
There are nearly 300 different proteins stored in platelet α-granules, such as CXCL1, platelet factor 4 (PF4), β-TG, CXCL5, CXCL7, CXCL12, macrophage inflammatory protein-1α (MIP-1α), and RANTES (CCL5), which play an important role in leukocyte infiltration and inflammatory response [60]
They carry a variety of granules and special structures like open canalicular system (OCS) and dense tubular system (DTS)
Summary
Asthma is a chronic and heterogeneous pulmonary disease which affects over 300 million people around the world [1]. Platelets are anucleate blood cells with a diameter of 2~4 μm generated from megakaryocytes They contain a variety of secretory granules, such as α-granules, dense granules (δ-granules), and lysosomes, which contain coagulation-related factors, and inflammatory mediators and protease [6]. Called atopic asthma, is the most common type of asthma with similar pathological features including mucus overproduction, chronic airway inflammation, airway remodeling, and airway hyperresponsiveness (AHR). It has been characterized as infiltration of eosinophils, mast cells, and lymphocytes in the airways and features increased secretion of type 2 cytokines such as IL-4, IL-5, and IL-13 after allergen exposure [13]. To provide a comprehensive understanding of the relationship between platelets and allergic asthma, we will elaborate on the following aspects: (i) the current understanding of platelets’ involvement in allergic asthma; (ii) the underlying mechanism of platelets’ role in the initiation of adaptive immunity and the pathogenic development of allergic asthma; (iii) the antiplatelet therapy in asthma treatment; and (iv) new insights on platelets in asthma
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