Glucagon-like Peptide-1 Receptor Pathway Attenuates Platelet Activation in Aspirin-Exacerbated Respiratory Disease
Open accessAbstract
Platelets are key contributors to allergic asthma and aspirin-exacerbated respiratory disease (AERD), an asthma phenotype involving platelet activation and IL-33–dependent mast cell activation. Human platelets express the glucagon-like peptide-1 receptor (GLP-1R). GLP-1R agonists decrease lung IL-33 release and airway hyperresponsiveness in mouse asthma models. We hypothesized that GLP-1R agonists reduce platelet activation and downstream platelet-mediated airway inflammation in AERD. GLP-1R expression on murine platelets was assessed using flow cytometry. We tested the effect of the GLP-1R agonist liraglutide on lysine-aspirin (Lys-ASA)–induced changes in airway resistance, and platelet-derived mediator release in a murine AERD model. We conducted a prospective cohort study comparing the effect of pretreatment with liraglutide or vehicle on thromboxane receptor agonist-induced in vitro activation of platelets from patients with AERD and nonasthmatic controls. GLP-1R expression was higher on murine platelets than on leukocytes. A single dose of liraglutide inhibited Lys-ASA–induced increases in airway resistance and decreased markers of platelet activation and recruitment to the lung in AERD-like mice. Liraglutide attenuated thromboxane receptor agonist-induced activation as measured by CXCL7 release in plasma from patients with AERD and CD62P expression in platelets from both patients with AERD (n = 31) and nonasthmatic, healthy controls (n = 11). Liraglutide, a Food and Drug Administration–approved GLP-1R agonist for treatment of type 2 diabetes and obesity, attenuates in vivo platelet activation in an AERD murine model and in vitro activation in human platelets in patients with and without AERD. These data advance the GLP-1R axis as a new target for platelet-mediated inflammation warranting further study in asthma.
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The primary outcome of GLP-1R expression involves suppressing the release of cytokines into the synovial fluid, leading to a reduction in inflammation.
“The primary outcome of GLP-1R expression involves suppressing the release of cytokines into the synovial fluid, leading to a reduction in inflammation.274,275”
From Glucagon-like peptide-1 receptor: mechanisms and advances in therapy (2024) · cites this paper as [275]
The Introduction (page unavailable) reports reduced lung cytokine production and markers of airway inflammation with GLP-1R agonist treatment. The Results section on AERD-like mice (page unavailable) reports reduced CXCL7 in bronchoalveolar lavage fluid. The paper does not support the claim about cytokine release into synovial fluid or establish that its suppression is the primary outcome of GLP-1R expression. (LLM, conf=0.84)
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- Authors
- Foer, D., Amin, T., Nagai, J., Tani, Y., Feng, C., Liu, T., Newcomb, D. C., Lai, J., Hayashi, H., Snyder, W. E., McGill, A., Lin, A., Laidlaw, T. M., Niswender, K. D., Boyce, J. A., & Cahill, K. N.
- Affiliations
- Brigham and Women's Hospital (US)
- Vanderbilt University Medical Center (US)
- Vanderbilt University (US)
- United States Department of Veterans Affairs (US)
- Corresponding author
- Cahill, Katherine N
- ORCID
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2023-10-23
- Volume
- 211
- Issue
- 12
- Pages
- 1806-1813
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC10842986
- OpenAlex
- W4387865495
- Cited by
- 17
- References
- 47
- Citations by year
- 2026: 8 · 2025: 4 · 2024: 5
- FWCI
- 3.00
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- HHS | NIH | National Heart, Lung, and Blood Institute (K23HL161332, R01HL117945)
- HHS | NIH | National Institute of Allergy and Infectious Diseases (K23AI118804, R37AI052353, R01AI136041, U19AI095219, U01AI155299)
- Topics
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Health Sciences › Medicine › Hematology › Platelet Disorders and Treatments
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Antiplatelet Therapy and Cardiovascular Diseases
- Keywords
- aspirin-exacerbated respiratory disease, GLP-1 receptor, liraglutide, platelet activation, IL-33, mast cell activation, airway hyperresponsiveness, CXCL7, P-selectin, allergic asthma
- MeSH terms
- Interleukin-33, Glucagon-Like Peptide-1 Receptor, Liraglutide, Animals, Aspirin, Asthma, Diabetes Mellitus, Type 2, Humans, Inflammation, Lysine, Prospective Studies, Platelet Activation, Receptors, Thromboxane, Mice, Asthma, Aspirin-Induced
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