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Steroid-Resistant Asthma and Neutrophils
1Laboratory of Immunopharmacology, Faculty of Pharmaceutical Sciences, Setsunan University.
Biological & Pharmaceutical Bulletin
|January 7, 2020
Summary
Steroid-resistant asthma involves neutrophils and NETosis, a specific cell death. This review explores how neutrophil activity contributes to severe asthma that doesn't respond to glucocorticoids.
Area of Science:
- Pulmonology
- Immunology
- Cell Biology
Background:
- Asthma is classified by phenotype and endotype, with most patients responding to glucocorticoids.
- Severe eosinophilic asthma (T-helper 2/type 2) and neutrophilic asthma (non-Th2/type 2) can be resistant to glucocorticoid therapy.
- Interleukin-33-induced type 2 innate lymphoid cells (ILC2) activation is glucocorticoid-resistant in some allergic conditions.
Purpose of the Study:
- To review the pathogenesis of steroid-resistant asthma.
- To focus on the role of neutrophils in steroid-resistant asthma.
- To explore the involvement of NETosis in asthmatic airway inflammation and steroid resistance.
Main Methods:
- Literature review of studies on asthma pathogenesis.
- Analysis of molecular pathways involved in steroid-resistant asthma.
- Focus on neutrophil-mediated inflammation and cell death (NETosis).
Main Results:
- Neutrophilic airway inflammation in steroid-resistant asthma involves IL-17, IL-8, and tumor necrosis factor-α.
- NETosis, a form of neutrophil cell death, is implicated in asthmatic airway inflammation.
- NETosis may contribute to the development and severity of steroid-resistant asthma.
Conclusions:
- Neutrophils and NETosis play a significant role in the pathogenesis of steroid-resistant asthma.
- Understanding these mechanisms could lead to new therapeutic strategies for difficult-to-treat asthma.
- Further research into neutrophil-targeted therapies is warranted for steroid-resistant asthma.
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