Platelet Dynamics in Asthma Pathophysiology

Platelets are increasingly recognised as dynamic contributors to the inflammatory and prothrombotic processes that underlie asthma. Beyond their classical role in haemostasis, activated platelets engage in chemotaxis, adhere to endothelium via P-selectin and integrins, and migrate into airway tissues. There, they form aggregates with eosinophils and other leukocytes, release mediators such as serotonin and platelet-derived growth factors, and amplify type 2 immune responses. These interactions promote bronchoconstriction, airway hyperresponsiveness and remodelling, and contribute to a systemic prothrombotic state marked by enhanced thrombin generation and impaired fibrinolysis. Emerging evidence also suggests that platelet metabolic adaptations and receptor-mediated recruitment pathways play critical roles in disease severity, exacerbation risk and potential therapeutic targeting.

Research from Nature Portfolio

A comprehensive meta-analysis has demonstrated that inhaled unfractionated heparin yields significant improvements in lung function in asthma, as measured by forced expiratory volume, and shows a favourable safety profile with minimal coagulopathy. Subgroup analyses indicate that dose, formulation and study design account for heterogeneity in treatment response, pointing towards optimised adjunctive strategies in chronic airway disease. Complementing this, a longitudinal cohort study linked prolonged clot lysis time and reduced levels of α2-macroglobulin at baseline with a higher incidence of severe asthma exacerbations over three years. These findings connect specific haemostatic alterations to clinical outcomes, underscoring the importance of disrupted fibrinolysis in asthma pathophysiology.

Platelet Dynamics in Asthma Pathophysiology publication trend

The graph below shows the total number of articles in platelet dynamics in asthma pathophysiology across all publications each year (not limited to Nature Index journals).

Technical terms

P-selectin: A cell-surface adhesion molecule on activated platelets that binds leukocyte ligands and mediates platelet-leukocyte interactions.

CCR3: A chemokine receptor expressed on platelets that directs their recruitment to inflamed airway tissue.

Fibrinolysis: The enzymatic process that dissolves fibrin clots, maintaining vascular patency.

α2-macroglobulin: A broad-spectrum protease inhibitor in plasma that regulates coagulation and fibrinolytic balance.

Monoamine oxidase B (MAO-B): An enzyme in platelets responsible for degradation of serotonin and other monoamines.

References

1. Platelets from Asthmatic Individuals Show Less Reliance on Glycolysis. PLOS ONE (2015).
2. Platelets Independently Recruit into Asthmatic Lungs and Models of Allergic Inflammation via CCR3. American Journal of Respiratory Cell and Molecular Biology (2021).
3. Efficacy and safety of inhaled heparin in asthmatic and chronic obstructive pulmonary disease patients: a systematic review and a meta-analysis. Scientific Reports (2023).
4. Impaired fibrinolysis and lower levels of plasma α2-macroglobulin are associated with an increased risk of severe asthma exacerbations. Scientific Reports (2017).
5. Emerging Roles of Platelets in Allergic Asthma. Frontiers in Immunology (2022).
6. Platelet Serotonin (5-HT) Concentration, Platelet Monoamine Oxidase B (MAO-B) Activity and HTR2A, HTR2C, and MAOB Gene Polymorphisms in Asthma. Biomolecules (2023).