Clinical Report: Targeted Approaches and Precision Diagnosis in Neutrophilic Asthma
Overview
Neutrophilic asthma is characterized by glucocorticoid resistance and severe disease. This review explores the molecular mechanisms involved, including the Th17/IL-17 axis and the role of neutrophil extracellular traps.
Background
Asthma affects over 300 million people globally, with 10-20% exhibiting neutrophilic inflammation. This phenotype is associated with more severe disease and poor response to conventional therapies.
Data Highlights
No numerical data or trial data provided in the source material.
Key Findings
Neutrophilic asthma is defined by sputum neutrophilia (≥61% neutrophils) and glucocorticoid resistance.
The Th17/IL-17 axis is central to neutrophil recruitment and activation in this asthma phenotype.
Neutrophil extracellular traps (NETs) contribute to airway damage and hyperresponsiveness.
The NLRP3 inflammasome amplifies inflammation through IL-1β and IL-18 release.
Airway microbiome dysbiosis is implicated in the pathogenesis of neutrophilic asthma.
Emerging therapies targeting IL-17, NET formation, and inflammasome components are in clinical development.
Clinical Implications
Clinicians should consider the distinct characteristics of neutrophilic asthma when evaluating treatment options, as traditional glucocorticoids may be ineffective.
Conclusion
This review provides a comprehensive understanding of neutrophilic asthma.
