Recent advances in understanding the roles of blood platelets in the pathogenesis of allergic inflammation and bronchial asthma.

Platelets play an essential role in hemostasis to minimize blood loss due to traumatic injury. In addition, they contain various immune-associated molecules and contribute to immunological barrier formation at sites of vascular injury, thereby protecting against invading pathogens. Platelets are also crucially involved in development of allergic diseases, including bronchial asthma. Platelets in asthmatics are more activated than those in healthy individuals. By using a murine asthma model, platelets were shown to be actively involved in progression of the disease, including in airway eosinophilia and airway remodeling. In the asthmatic airway, pathological microvascular angiogenesis, a component of airway remodeling, is commonly observed, and the degree of abnormality is significantly associated with disease severity. Therefore, in order to repair the newly formed and structurally fragile blood vessels under inflammatory conditions, platelets may be continuously activated in asthmatics. Importantly, platelets constitutively express IL-33 protein, an alarmin cytokine that is essential for development of bronchial asthma. Meanwhile, the concept of development of allergic diseases has recently changed dramatically, and allergy researchers now share a belief in the centrality of epithelial barrier functions. In particular, IL-33 released from epithelial barrier tissue at sites of eczema can activate the antigen-non-specific innate immune system as an alarmin that is believed to be necessary for subsequent antigen-specific acquired immunological responses. From this perspective, we propose in this review a possible mechanism for how activated platelets act as an alarmin in development of bronchial asthma.