Abstract
Several recent studies spanning from induced sputum to gene signature identified non-eosinophilic asthma (NEA) as a distinct asthma phenotype with several relevant clinical features such as increased asthma severity, increased remodelling and lower response to bronchodilator and anti-inflammatory treatment. Two major mechanisms leading to neutrophilic inflammation are postulated: the dysregulated innate immune response, including neutrophil intrinsic abnormalities, and the activation of the IL-17-dependent pathway. Several factors such as age, metabolic or epigenetic factors or the activation of the epithelial-mesenchimal trophic unit have been identified as modulators. The endotyping of NEA is far behind the eosinophilic asthma, and until now, no endotype-driven interventions have been proved to be effective.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
