Platelets are anucleate blood cells, long known to be critically involved in hemostasis and thrombosis. In addition to their role in blood clots, increasing evidence reveals significant roles for platelets in inflammation and immunity. However, the notion that platelets represent immune cells is not broadly recognized in the field of Physiology. This article reviews the role of platelets in inflammation and immune responses, and highlights their interactions with other immune cells, including examples of major functional consequences of these interactions. Published 2015. Compr Physiol 5:1265-1280, 2015.

/pdf/platelets-and-their-interactions-with-other-immune-cells-14iwmqpdxj.pdf

Platelets and Their Interactions with Other Immune Cells.

Hypereosinophilic syndromes (HESs) are a diverse group of conditions characterized by clinical manifestations attributable to eosinophilia and eosinophilic infiltration of tissues. HESs are chronic disorders with significant morbidity and mortality. Although the availability of targeted chemotherapeutic agents, including imatinib, has improved quality of life and survival in some patients with HESs, additional agents with increased efficacy and decreased toxicity are sorely needed. The purpose of this review is to provide an overview of eosinophil biology with an emphasis on potential targets of pharmacotherapy and to provide a summary of potential eosinophil-targeting agents, including those in development, in clinical trials, or approved for other disorders. (J Allergy Clin Immunol 2012;130:563-71.)

https://www.jacionline.org/article/S0091-6749(12)01205-5/pdf

Clinical reviews in allergy and immunology

Rationale: Eosinophil β1-integrin activation correlates inversely with FEV1 and directly with eosinophil-bound P-selectin in subjects with nonsevere allergic asthma.Objectives: Determine the relationships between β1-integrin activation and pulmonary function or eosinophil-bound P-selectin in subjects with asthma of varying severity and discern the source of eosinophil-bound P-selectin.Methods: Blood was assayed by flow cytometry for P-selectin and activated β1-integrin on eosinophils and platelets. Plasma was analyzed with ELISA for soluble P-selectin, platelet factor 4, and thrombospondin-1.Measurements and Main Results: Activated β1-integrin correlated with eosinophil-bound P-selectin among all subjects with asthma even though activated β1-integrin was higher in subjects with nonsevere asthma than severe asthma. Activated β1-integrin correlated inversely with FEV1 corrected for FVC only in younger subjects with nonsevere asthma. Paradoxically, platelet surface P-selectin, a platelet activation marker, w...

/pdf/platelet-activation-p-selectin-and-eosinophil-b1-integrin-1y45lhzpjz.pdf

Platelet Activation, P-Selectin, and Eosinophil β1-Integrin Activation in Asthma

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 preformed mediators of inflammation that are released on activation and are a rich source of newly synthesized lipid mediators that alter vascular permeability and smooth muscle tone. Accordingly, platelet activity 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 asthmatic patients in general and in patients with AERD in particular and considers the potential therapeutic implications.

/pdf/platelets-in-patients-with-aspirin-exacerbated-respiratory-2tu0cbwqqo.pdf

Platelets in patients with aspirin-exacerbated respiratory disease

Platelets have the capacity to release mediators with potent inflammatory or anaphylactic properties Platelet factor-4 (PF4) and beta-thromboglobulin (BTG) are two of these mediators On the other hand, plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA) are two important mediators of fibrinolysis Both mediators are secreted mainly by vascular endothelium Plasma levels of PF4, BTG, PAI-1, and tPA may show changes in chronic inflammatory diseases such as asthma This study examined the role of thrombocytes and the function of the endothelium in asthmatic patients during an attack and during a stable phase Eighteen patients with known allergic asthma who came to our emergency department with an asthma attack and 14 control subjects were included in the study Blood samples were taken after starting therapy with salbutamol inhalation Lung function tests were performed after receiving the first emergency therapy for asthma Plasma levels of PF4, BTG, PAI-1, tPA were determined before starting steroid therapy and after receiving 1 week of steroid therapy Plasma levels of PF4 among patients with an asthma attack were significantly higher than those of controls (1505+/-892 IU/mL vs 925+/-763 IU/mL, p<0001) A further increase in plasma PF4 levels was detected after steroid therapy (1635+/-916 IU/mL) Plasma BTG levels of patients on admission were not statistically different from those in the control group (1404+/-634 IU/mL vs 1522+/-871 IU/mL) An increase was detected after therapy (1716+/-727 IU/mL) and post-treatment plasma levels were statistically meaningful versus the controls Plasma levels of tPA and PAI were statistically higher than those in controls in asthmatic patients on admission (601+/-272 vs 54+/-23 ng/mL for tPA and 752+/-272 ng/mL vs 327+/-143 ng/mL for PAI-1) Further increases were detected in two parameters after 1 week of therapy with steroids (tPA levels were 685+/-296 ng/mL and PAI-1 levels were 835+/-296 ng/mL) There seems to be an increased activity of platelets during an asthma attack Elevated PAI-1 and tPA levels may also indicate the activated endothelium in asthma Increases of plasma levels of PAI-1 and tPA after steroid therapy need further investigation because elevated PAI-1 levels enhance airway remodeling

https://journals.sagepub.com/doi/pdf/10.1177/107602960501100109

Platelet Function and Fibrinolytic Activity in Patients with Bronchial Asthma

Peak expiratory flow (PEF) and plasma concentrations of platelet factor 4 and beta thromboglobulin were measured before and after exercise in nine asthmatic patients and 12 non-asthmatic volunteers. Exercise was preceded by administration in random order of either placebo, salbutamol 200 micrograms, or sodium cromoglycate 2 mg from a pressurised inhaler. In control subjects there were minimal changes in PEF and plasma concentrations of platelet factor 4 and beta thromboglobulin. In the asthmatic patients the typical changes in PEF were seen on exercise; plasma concentrations of platelet factor 4 and beta thromboglobulin rose significantly in parallel, the rise preceding the fall in PEF. The changes in peak flow and platelet activation induced by exercise were attenuated by prior administration of salbutamol or cromoglycate. These results indicate that exercise induced asthma is associated with a rise in platelet release products similar to that observed in antigen induced asthma.

https://thorax.bmj.com/content/thoraxjnl/41/4/290.full.pdf

Platelet activation during exercise induced asthma: effect of prophylaxis with cromoglycate and salbutamol.

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Platelet activation during exercise induced asthma: effect of prophylaxis with cromoglycate and salbutamol.