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Fibrocyte localisation to the ASM bundle in asthma: bidirectional effects on cell phenotype and behaviour
Ruth Saunders1, Davinder Kaur1, Dhananjay Desai1,2
1Department of Respiratory Sciences Institute for Lung Health University of Leicester Leicester UK.
Clinical & Translational Immunology
|November 19, 2020
Summary
Fibrocytes accumulate in airway smooth muscle (ASM) in asthma, contributing to airway hyperresponsiveness. Understanding fibrocyte recruitment to ASM may reveal new asthma treatment targets.
Area of Science:
- Respiratory Medicine
- Immunology
- Cell Biology
Background:
- Airway hyper-responsiveness and airflow obstruction are key in asthma.
- Airway smooth muscle (ASM) hypercontractility and increased mass contribute to asthma.
- Fibrocytes are implicated in asthma pathogenesis, localizing to ASM.
Purpose of the Study:
- To investigate fibrocyte localization in ASM in nonasthmatic eosinophilic bronchitis (NAEB) and chronic obstructive pulmonary disease (COPD).
- To explore the consequences of fibrocyte localization to ASM in asthma pathophysiology.
- To examine the in vitro effects of fibrocytes on ASM phenotype and behavior.
Main Methods:
- Immunohistochemistry to enumerate fibrocytes and proliferating cells in bronchial ASM.
- In vitro co-culture assays to assess ASM and fibrocyte interactions (cell number, size, apoptosis, phenotype, contractility).
Main Results:
- Increased fibrocyte numbers in ASM were observed in asthma compared to NAEB and controls.
- ASM proliferation in vivo was not different between asthmatics and controls.
- Co-culture studies showed enhanced fibrocyte smooth muscle marker expression and collagen gel contraction with asthmatic ASM, suggesting a role in asthma pathogenesis.
Conclusions:
- Fibrocyte accumulation in ASM is specific to asthma.
- Further research into fibrocyte recruitment and differentiation in ASM is crucial for identifying novel therapeutic targets.
- Modulating ASM dysfunction through targeting fibrocytes holds potential for asthma treatment.
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