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10.1016/j.jaci.2015.02.005

http://scihub22266oqcxt.onion/10.1016/j.jaci.2015.02.005
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C4559084!4559084!26051947
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suck abstract from ncbi

pmid26051947      J+Allergy+Clin+Immunol 2015 ; 135 (6): 1407-15
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  • Platelets in aspirin-exacerbated respiratory disease #MMPMID26051947
  • Laidlaw TM; Boyce JA
  • J Allergy Clin Immunol 2015[Jun]; 135 (6): 1407-15 PMID26051947show ga
  • Aspirin-exacerbated respiratory disease (AERD) is a chronic inflammatory disease characterized clinically by the triad of asthma, nasal polyposis, and pathognomonic respiratory reactions after ingestion of aspirin. It is a distinct syndrome associated with eosinophilic infiltration of respiratory tissues and excessive production of cysteinyl leukotrienes. Despite the consistent clinical phenotype of the respiratory disease, the underlying pathogenesis of the disease remains unclear. In addition to their role in hemostasis, platelets have the capacity to influence the activation state and function of other immune cells during inflammation, and to facilitate granulocyte recruitment into the tissues. Platelets also possess a repertoire of potent pre-formed mediators of inflammation that are released upon activation, and are a rich source of newly-synthesized lipid mediators that alter vascular permeability and smooth muscle tone. Accordingly, the activity of platelets has been linked to diverse inflammatory diseases, including asthma. Both human and animal studies strongly suggest that platelet activity is uniquely associated with the pathophysiology of AERD. This article summarizes the evidence supporting an effector role for platelets in asthma in general and in AERD in particular, and considers the potential therapeutic implications.
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