Abstract

Asthma is a complex chronic airway disease with several distinct phenotypes characterized by different immunopathological pathways, clinical presentation, physiology, comorbidities, biomarker of allergic inflammation, and response to treatment. Approximately 10% of patients with asthma have severe refractory disease, which is difficult to control on high doses of inhaled corticosteroids and other modifiers. About 50% of these individuals suffer from neutrophilic asthma.

Highlights

  • Asthma is a complex chronic airway disease with several distinct phenotypes characterized by different immunopathological pathways, clinical presentation, physiology, comorbidities, biomarker of allergic inflammation, and response to treatment [1,2,3,4]

  • Neutrophilic asthma is a complex phenotype of asthma that is severe and persistent, with frequent exacer

  • Interleukin-23 plays a pivotal role in the development and maintenance of T helper 17 (Th17) cells which produce IL-17

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Summary

Introduction

Asthma is a complex chronic airway disease with several distinct phenotypes characterized by different immunopathological pathways, clinical presentation, physiology, comorbidities, biomarker of allergic inflammation, and response to treatment [1,2,3,4]. Interleukin-17 is produced mainly by Th17 cells, but other cells in the lung can secrete the IL-17 family members It plays a key role in the pathogenesis of neutrophilic asthma by expressing the secretion of chemoattractant cytokines, chemokines, and adhesion molecules which lead to the recruitment, and activation of neutrophils. Ciprandi and colleagues [42,43] have found that serum IL-23 levels were increased in allergic asthmatic children not on corticosteroids treatment, compared

Airway remodeling
Activated Neutrophils in Neutrophilic Asthma
Role of NETosis in Neutrophilic Asthma
Findings
Conclusion
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