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S100A12 and the Airway Smooth Muscle: Beyond Inflammation and Constriction
Blanca Camoretti-Mercado1, Eltayeb Karrar1, Luis Nuñez2
1Department of Medicine, Section of Pulmonary and Critical Care, University of Chicago, USA.
Journal of Allergy & Therapy
|May 19, 2015
Summary
Airway Smooth Muscle (ASM) abundance drives airway hyperresponsiveness (AHR) in asthma and COPD. The protein S100A12 can reduce ASM amounts and inflammation, offering a potential therapeutic target for AHR.
Area of Science:
- Pulmonary Medicine
- Immunology
- Cell Biology
Background:
- Airway inflammation, lung remodeling, and Airway Hyperresponsiveness (AHR) are key features of asthma and Chronic Obstructive Pulmonary Disease (COPD).
- Airway Smooth Muscle (ASM) overabundance contributes to lung structural changes and AHR, with emerging evidence suggesting ASM, not inflammation, is the primary driver of AHR.
- S100/calgranulins family members, including S100A12, are implicated in inflammation and apoptosis regulation.
Purpose of the Study:
- To investigate the role of S100A12 in regulating airway smooth muscle (ASM) mass and airway hyperresponsiveness (AHR).
- To explore the potential of targeting ASM with pro-apoptotic S100A12 as a therapeutic strategy for asthma and COPD.
Main Methods:
- Utilized genetically engineered mice with smooth muscle cell-targeted expression of human S100A12.
- Evaluated the effects of S100A12 on ASM abundance, airway inflammation, and AHR in a model of allergic lung inflammation.
Main Results:
- S100A12 expression in ASM reduced ASM amounts.
- S100A12 significantly dampened airway inflammation and airway hyperreactivity in the allergic lung inflammation model.
- S100A12 demonstrated pro-apoptotic effects on ASM.
Conclusions:
- Airway Smooth Muscle (ASM) is a critical determinant of Airway Hyperresponsiveness (AHR).
- S100A12 effectively reduces ASM mass and ameliorates airway inflammation and AHR.
- Targeting ASM with pro-apoptotic agents like S100A12 presents a promising therapeutic avenue for asthma and COPD.
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