Asthma is a prevalent pulmonary disease that affects more than 300 million people worldwide and imposes a substantial economic burden. While medication can effectively control symptoms in some patients, severe asthma attacks, driven by airway inflammation induced by environmental and infectious exposures, continue to be a major cause of asthma-related mortality. Heterogeneous phenotypes of asthma include type 2 (T2) and non-T2 asthma. Non-T2 asthma is often observed in patients with severe and/or steroid-resistant asthma. This review covers the molecular mechanisms, clinical phenotypes, causes and promising treatments of non-T2 severe asthma. Specifically, we discuss the signalling pathways for non-T2 asthma including the activation of inflammasomes, interferon responses and interleukin-17 pathways, and their contributions to the subtypes, progression and severity of non-T2 asthma. Understanding the molecular mechanisms and genetic determinants underlying non-T2 asthma could form the basis for precision medicine in severe asthma treatment.
Keyphrases
- chronic obstructive pulmonary disease
- lung function
- allergic rhinitis
- air pollution
- end stage renal disease
- cystic fibrosis
- emergency department
- cardiovascular disease
- gene expression
- coronary artery disease
- dna methylation
- depressive symptoms
- chronic kidney disease
- ejection fraction
- newly diagnosed
- peritoneal dialysis
- physical activity
- genome wide
- electronic health record
- drug induced
- human health