Type 2 inflammation, a common denominator in chronic airway disease?

This review addresses the growing understanding that a specific subset of patients with a respiratory disease, including asthma, chronic obstructive pulmonary disease (COPD), or bronchiectasis may have one thing in common: type 2 inflammation. In the era of personalized medicine, we need to refine clinical markers combined with molecular and cellular endotyping to improve patient outcomes.

Recent literature reveals that type 2 markers such as blood eosinophils, fractional exhaled nitric oxide (FeNO), and immunglobulin E (IgE), can provide valuable insights into disease progression, exacerbation risk, and treatment response, but their stability remains to be investigated. Treating asthma and COPD patients with biologics to target IL-4/IL-13, IL-5, and alarmins have shown potential, although efficacy varied. In bronchiectasis, a subset of patients with type 2 inflammation may benefit from corticosteroid therapy, despite broader concerns regarding its use.

This underscores the importance of improved disease endotyping to better characterize patients who may benefit from targeted therapies. In clinical practice, personalized treatment based on inflammatory profiles has been shown to improve outcomes in heterogeneous lung diseases. Future research needs to focus on validating reliable biomarkers and optimizing clinical trial designs to advance therapeutic strategies in respiratory diseases.