Eosinophil Activation and Airway Inflammation in Allergic Disorders
Summary
Allergic disorders of the airways, including asthma and allergic rhinitis, are characterised by type-2 immune responses that culminate in the recruitment, activation and persistence of eosinophils within bronchial tissues. Eosinophils are granulocytic leukocytes armed with cytotoxic proteins and a repertoire of cytokines and lipid mediators. Activation typically follows epithelial release of alarmin cytokines (for example IL-33 and thymic stromal lymphopoietin) and the generation of chemotactic signals such as eotaxins. Circulating eosinophils adhere to activated endothelium via integrins, extravasate and migrate through the extracellular matrix under the influence of interleukin-5 (IL-5) and other growth factors. Within the airway, degranulation releases major basic protein, eosinophil peroxidase and reactive mediators that damage epithelium, promote airway hyperresponsiveness and drive structural remodelling through interactions with fibroblasts. Persistent eosinophilic inflammation correlates with exacerbation risk, airflow obstruction and steroid-resistant disease. Recent advances in monoclonal therapies targeting IL-5, IL-5 receptor and alarmin pathways have underscored the central role of eosinophils in pathogenesis and opened avenues for precision medicine in severe allergic airway disease.
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Eosinophil Activation and Airway Inflammation in Allergic Disorders publication trend
The graph below shows the total number of articles in eosinophil activation and airway inflammation in allergic disorders across all publications each year (not limited to Nature Index journals).
Technical terms
Eosinophil: A type of white blood cell containing cytotoxic granules; central effector in type-2 immune responses and allergic inflammation.
Interleukin-5 (IL-5): A cytokine essential for eosinophil growth, differentiation and survival; principal target of several biologic therapies.
Alarmin: An epithelial-derived cytokine (for example IL-33, TSLP) released upon barrier disruption that activates innate and adaptive type-2 immunity.
Eosinophil-lineage-committed progenitor (EoP): A bone marrow–derived CD34+ cell that gives rise specifically to eosinophils and may localise to inflamed lung tissue for in situ differentiation.
Interleukin-1α (IL-1α): A pro-inflammatory cytokine released by damaged or activated cells, here implicated in eosinophil-driven activation of airway fibroblasts.
References
- Monoclonal antibody therapy for the treatment of asthma and chronic obstructive pulmonary disease with eosinophilic inflammation. Pharmacology & Therapeutics (2016).
- Eosinophil Lineage-Committed Progenitors as a Therapeutic Target for Asthma. Cells (2021).
- Interleukin-1α Is a Critical Mediator of the Response of Human Bronchial Fibroblasts to Eosinophilic Inflammation. Cells (2021).
- Comparison of IL-33 and IL-5 family mediated activation of human eosinophils. PLOS ONE (2019).
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