Eosinophil Recruitment Mechanisms in Airway Inflammation

Eosinophils are specialised granulocytes whose accumulation in the airways underlies the pathology of asthma, chronic rhinosinusitis and other eosinophilic disorders. Following allergen exposure or viral insult, airway epithelial cells and resident dendritic cells release “alarmins” such as interleukin-33, which activate type‐2 immune pathways. Group 2 innate lymphoid cells (ILC2) and T helper 2 lymphocytes then secrete interleukin-5 and interleukin-13, driving eosinophil maturation in the bone marrow and priming the endothelium for leukocyte adhesion. Concurrent upregulation of adhesion molecules (VCAM-1, selectins) supports eosinophil tethering and rolling. A cascade of CC chemokines—including eotaxins (CCL11, CCL24, CCL26), CCL13 and CCL7—creates a transendothelial gradient that engages eosinophil-selective receptors (CCR3, CCR9) and directs chemotaxis into the airway tissue. Within the inflamed mucosa, local production of bioactive lipids and survival factors sustains eosinophil activation, degranulation and cytokine release. Dysregulated recruitment amplifies airway hyperresponsiveness, mucus hypersecretion and tissue remodelling. Detailed insights into chemokine–receptor interactions, adhesion cascades and lipid mediators are now informing targeted strategies to interrupt eosinophil influx and resolve airway inflammation.

Research from Nature Portfolio

Recent studies have demonstrated the therapeutic potential of chemokine‐receptor blockade to curb eosinophil migration. A novel small‐molecule antagonist of CCR4 was shown to inhibit binding of its ligands, leading to profound reductions in airway eosinophilia, type 2 cytokines and bronchial hyperreactivity in a murine ovalbumin challenge model. This proof-of-concept exemplifies how selective receptor inhibition can attenuate hallmark features of allergic airway inflammation and suggests a template for targeting other chemokine axes involved in eosinophil homing.

Eosinophil Recruitment Mechanisms in Airway Inflammation publication trend

The graph below shows the total number of articles in eosinophil recruitment mechanisms in airway inflammation across all publications each year (not limited to Nature Index journals).

Technical terms

Eosinophil: A type of white blood cell containing cytotoxic granules, central to defence against parasites and promotion of allergic inflammation.

Chemokine: A small signalling protein that directs leukocyte migration along concentration gradients.

Chemokine receptor: A G protein-coupled receptor on leukocytes that binds specific chemokines to initiate cell movement.

Eotaxin: Members of the CC chemokine family (CCL11, CCL24, CCL26) that selectively attract eosinophils.

Type 2 cytokines: Immune signalling proteins—including IL-4, IL-5 and IL-13—that orchestrate allergic inflammation.

Group 2 innate lymphoid cell (ILC2): An innate immune cell subset that rapidly produces type 2 cytokines and amplifies eosinophil recruitment.

References

1. CCL13 and human diseases. Frontiers in Immunology (2023).
2. Regulation of Eosinophil and Group 2 Innate Lymphoid Cell Trafficking in Asthma. Frontiers in Medicine (2017).
3. CCR9 Is a Key Regulator of Early Phases of Allergic Airway Inflammation. Mediators of Inflammation (2016).
4. A new antagonist for CCR4 attenuates allergic lung inflammation in a mouse model of asthma. Scientific Reports (2017).