Abstract
Although 2 T-helper type 2 inflammation evokes airway hyperresponsiveness and narrowing, neutrophilic or pauci-immune asthma accounts for significant asthma morbidity. Viruses, toxicants, environmental tobacco smoke exposure, and bacterial infections induce asthma exacerbations mediated by neutrophilic inflammation or by structural cell (pauci-immune) mechanisms. Therapeutic challenges exist in the management of neutrophilic and pauci-immune phenotypes because both syndromes manifest steroid insensitivity. The recognition that neutrophil subsets exist and their functions are unique poses exciting opportunities to develop precise therapies. The conventional thought to target neutrophil activation or migration globally may explain why current drug development in neutrophilic asthma remains challenging.
Original language | English (US) |
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Pages (from-to) | 569-579 |
Number of pages | 11 |
Journal | Immunology and Allergy Clinics of North America |
Volume | 36 |
Issue number | 3 |
DOIs | |
State | Published - Aug 1 2016 |
Externally published | Yes |
All Science Journal Classification (ASJC) codes
- Immunology and Allergy
- Immunology
Keywords
- Airway remodeling
- Intrinsic asthma
- Irreversible airway obstruction
- Nonatopic asthma
- Steroid insensitivity