The onset, development and pathogenesis of severe neutrophilic asthma
Bronchial asthma is divided into Th2 high, Th2 low and mixed types. The Th2 high type is dominated by eosinophils while the Th2 low type is divided into neutrophilic and paucigranulocytic types. Eosinophilic asthma has gained increased attention recently, and its pathogenesis and treatment are well...
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Veröffentlicht in: | Immunology and cell biology 2022-03, Vol.100 (3), p.144-159 |
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Sprache: | eng |
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Zusammenfassung: | Bronchial asthma is divided into Th2 high, Th2 low and mixed types. The Th2 high type is dominated by eosinophils while the Th2 low type is divided into neutrophilic and paucigranulocytic types. Eosinophilic asthma has gained increased attention recently, and its pathogenesis and treatment are well understood. However, severe neutrophilic asthma requires more in‐depth research because its pathogenesis is not well understood, and no effective treatment exists. This review looks at the advances made in asthma research, the pathogenesis of neutrophilic asthma, the mechanisms of progression to severe asthma, risk factors for asthma exacerbations, and biomarkers and treatment of neutrophilic asthma. The pathogenesis of neutrophilic asthma is further discussed from four aspects: Th17‐type inflammatory response, inflammasomes, exosomes and microRNAs. This review provides direction for the mechanistic study, diagnosis and treatment of neutrophilic asthma. The treatment of neutrophilic asthma remains a significant challenge for clinical therapists and is an important area of future clinical research.
Neutrophilic asthma is asthma in which neutrophils are predominantly increased. This review looks at the advances made in asthma research, the pathogenesis of neutrophilic asthma, the mechanism of progression to severe asthma, risk factors for asthma exacerbations, and biomarkers and treatment of neutrophilic asthma. This review provides direction for the prevention, diagnosis and treatment of severe asthma. |
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ISSN: | 0818-9641 1440-1711 |
DOI: | 10.1111/imcb.12522 |