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Glucocorticoids preferentially upregulate functional CXCR4 expression in eosinophils.

H Nagase¹, M Miyamasu, M Yamaguchi

¹Department of Respiratory Medicine, University of Tokyo Graduate School of Medicine, Tokyo, Japan.

The Journal of Allergy and Clinical Immunology

|December 12, 2000

Summary

Glucocorticoids (GCCs) increase eosinophil CXCR4 expression, potentially explaining their anti-allergic effects by shifting eosinophils to tissues. This study reveals a novel mechanism for GCCs in managing allergic inflammation.

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Area of Science:

Immunology
Cell Biology
Pharmacology

Background:

Chemokines are crucial for eosinophil accumulation in allergic inflammation.
Glucocorticoids (GCCs) reduce tissue eosinophilia, but their effect on eosinophil chemokine receptor expression is unknown.
GCCs are known to inhibit chemokine production, but not receptor regulation on eosinophils.

Purpose of the Study:

To investigate how GCCs regulate chemokine receptor expression on eosinophils.
To understand the functional consequences of GCC-induced changes in eosinophil chemokine receptor expression.

Main Methods:

Flow cytometry and reverse transcriptase PCR were used to analyze chemokine receptor expression.
Intracellular calcium influx and chemotaxis assays were performed.
Dexamethasone (DEX) was used as the model GCC.

Main Results:

Dexamethasone (DEX) slightly downregulated CCR3 expression on eosinophils.
DEX significantly upregulated CXCR4 expression on eosinophils in a time- and dose-dependent manner (approx. 6-fold increase).
Neutrophil CXCR4 expression was only marginally affected by DEX, and CXCR4 ligand (SDF-1α) induced greater Ca2+ influx and chemotaxis in DEX-treated eosinophils.

Conclusions:

GCCs upregulate CXCR4 expression in eosinophils, but not neutrophils.
Upregulation of CXCR4 by GCCs may contribute to their anti-allergic properties by sequestering eosinophils in extravascular tissues.
This mechanism suggests a role for CXCR4 in the baseline trafficking of eosinophils, rather than direct recruitment to inflammatory sites.