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Published on: April 16, 2019
Airway smooth muscle chemokine receptor expression and function in asthma
R Saunders1, A Sutcliffe, D Kaur
1Department of Infection, Immunity and Inflammation, Institute for Lung Health, University of Leicester, Leicester, UK.
Summary
Chemokine receptors CXCR1, 3, and 4 are expressed by airway smooth muscle (ASM) cells and influence wound healing. However, their specific role in asthma remains unclear, as no differences were found between asthmatic and non-asthmatic individuals.
Area of Science:
- Immunology
- Cell Biology
- Respiratory Medicine
Background:
- Chemokine receptors are crucial for cell migration and wound repair.
- CCR3 and CCR7 are known to be expressed by airway smooth muscle (ASM) cells, with CCR7 linked to ASM hyperplasia in asthma.
- Further investigation into other chemokine receptor expression and function in ASM is needed.
Purpose of the Study:
- To explore the expression profile of chemokine receptors on ASM cells.
- To determine the functional roles of these receptors in ASM cells, particularly in the context of asthma.
Main Methods:
- ASM cells were obtained from individuals with and without asthma.
- Chemokine receptor expression was analyzed using flow cytometry and immunofluorescence.
- Functional assays included intracellular calcium measurements, chemotaxis, wound healing, proliferation, and survival.
Main Results:
- CXCR1, CXCR3, and CXCR4 were highly expressed on ASM cells, alongside CCR3 and CCR7.
- These CXC chemokine receptors were functional, increasing intracellular calcium and promoting wound healing.
- CXCR3 inhibition impaired spontaneous wound healing, but receptor activation did not affect ASM chemotaxis, proliferation, or survival.
- No significant differences in receptor expression or function were observed between asthmatic and non-asthmatic ASM cells.
Conclusions:
- CXCR1, CXCR3, and CXCR4 are expressed by ASM cells and can modulate certain ASM functions, including wound healing.
- The precise clinical significance of these receptors in asthma pathogenesis is currently uncertain.
- The study found no difference in ASM chemokine receptor expression or function between asthmatic and non-asthmatic subjects.
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