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Refractory asthma: mechanisms, targets, and therapy.
1Division of Pulmonary Allergy and Critical Care Medicine, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, USA.
Allergy
|April 30, 2014
Summary
Inhaled corticosteroids (ICS) are recommended for asthma, but steroid resistance can occur. Understanding mechanisms like Th17 pathways and oxidative stress is key to developing new treatments for severe asthma.
Area of Science:
- Pulmonology
- Immunology
- Molecular Biology
Background:
- Asthma affects 300 million globally, characterized by airway inflammation and obstruction.
- Inhaled corticosteroids (ICS) are standard treatment, targeting gene transcription via the glucocorticoid receptor (GR).
- Alternative asthma phenotypes, like Th17-mediated neutrophil-predominance, may exhibit steroid resistance.
Purpose of the Study:
- To explore the molecular mechanisms underlying glucocorticoid resistance in asthma.
- To identify factors contributing to steroid unresponsiveness in severe asthma cases.
Main Methods:
- Review of current literature on asthma pathophysiology and glucocorticoid receptor signaling.
- Analysis of mechanisms involving Th17 pathways, GR phosphorylating kinases, and oxidative stress.
Main Results:
- Glucocorticoid resistance can stem from altered GR-transcription factor interactions due to kinase activity.
- Oxidative stress impacts gene transcription balance by inhibiting histone deacetylase 2.
- Th17-mediated inflammation presents a phenotype potentially less responsive to steroids.
Conclusions:
- Understanding glucocorticoid resistance mechanisms is crucial for advancing asthma treatment.
- Novel therapeutic strategies targeting these pathways could improve outcomes for severe, refractory asthma.
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