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CCR3 expression and function in asthmatic airway smooth muscle cells
Philippe Joubert1, Stéphane Lajoie-Kadoch, Isabelle Labonté
1Meakins-Christie Laboratories, McGill University, Montréal, Québec, Canada.
Journal of Immunology (Baltimore, Md. : 1950)
|August 6, 2005
Summary
Airway smooth muscle cells (ASMC) express CCR3, a receptor involved in immune responses. This study found higher CCR3 expression in asthmatic patients, suggesting eotaxin
Area of Science:
- Immunology
- Respiratory Medicine
- Cell Biology
Background:
- Asthma involves increased airway smooth muscle mass.
- Airway smooth muscle cells (ASMC) express immune receptors.
- CCR3 receptor's role in ASMC is not fully understood.
Purpose of the Study:
- Examine CCR3 expression on ASMC.
- Compare CCR3 expression in asthmatic vs. non-asthmatic subjects.
- Determine CCR3's role in ASMC migration.
Main Methods:
- ASMC cultured and stimulated with TNF-alpha.
- Flow cytometry (FACS) for CCR3 expression analysis.
- Calcium assays and chemotaxis assays for functional assessment.
Main Results:
- ASMC constitutively express CCR3 mRNA and protein.
- TNF-alpha significantly increased surface CCR3 expression.
- Higher CCR3 expression observed in asthmatic ASMC (95%) vs. controls (75%).
- Eotaxin (CCR3 ligand) induced ASMC calcium production and chemotaxis.
- ASMC migration increased 2.2-fold towards eotaxin.
Conclusions:
- ASMC express functional CCR3, with increased expression in asthmatics.
- Eotaxin-induced ASMC migration via CCR3 may contribute to airway remodeling in asthma.
- CCR3 and its ligand eotaxin are potential therapeutic targets for asthma.