Eosinophil Adhesion Mechanisms in Asthmatic Inflammation

Eosinophil adhesion to the vascular endothelium and subsequent transmigration into the airway mucosa represent critical steps in the pathophysiology of asthma. These processes are orchestrated by a coordinated interplay between adhesion molecules, including integrins and selectins, chemokines such as eotaxins, and mechanical forces arising from blood flow. Upon activation by Th2-type mediators, eosinophils upregulate high-affinity conformations of α4β1 and αMβ2 integrins, enabling firm adhesion to endothelial intercellular adhesion molecule-1 and vascular cell adhesion molecule-1. Selectins mediate the initial tethering and rolling phases, while chemokine-induced intracellular calcium flux triggers cytoskeletal rearrangement and actin polymerisation, facilitating transendothelial migration. Dysregulated adhesion dynamics contribute to persistent airway inflammation, mucus hypersecretion and tissue remodelling, underscoring the global significance of targeting eosinophil adhesion pathways in the management of severe asthma and the development of novel anti-adhesion therapies.

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Technical terms

Integrins: transmembrane heterodimeric receptors that mediate firm adhesion of leukocytes to endothelial cells by binding to extracellular matrix proteins and cell-adhesion molecules.

Selectins: family of C-type lectins responsible for the initial tethering and rolling of leukocytes on vascular endothelium under shear flow.

Chemokines: small secreted proteins that guide leukocyte migration by binding to G-protein coupled receptors and activating intracellular signalling pathways.

Mechanotransduction: process by which cells convert mechanical stimuli, such as fluid shear stress, into biochemical signals that regulate cellular behaviour.

Transmigration: multistep passage of leukocytes across the endothelial barrier into surrounding tissues, involving adhesion, cytoskeletal rearrangement and junctional opening.

Actin polymerisation: dynamic assembly of actin filaments that drives morphological changes necessary for cell movement and adhesion.

References

1. The Cycling of Intracellular Calcium Released in Response to Fluid Shear Stress Is Critical for Migration-Associated Actin Reorganization in Eosinophils. Cells (2021).
2. Triple selectin knockout (ELP-/-) mice fail to develop OVA-induced acute asthma phenotype. Journal of Inflammation (2011).