Bronchiectasis is a heterogeneous chronic airway disease traditionally viewed as neutrophil-driven. Emerging evidence demonstrates distinct complex inflammatory phenotypes influencing clinical outcomes, prognosis and therapeutic options. A narrative review was conducted, informed by a structured literature search on PubMed and Google Scholar databases, focusing on inflammatory phenotypes in bronchiectasis. Based on the prevalent cellular population, four distinct phenotypes can be described. The most common is the neutrophilic phenotype, which is associated with frequent Pseudomonas infection, severe disease, exacerbations and poor prognosis. Targeted novel-agents for this group such as brensocatib (neutrophil protease inhibition) emerge. The eosinophilic phenotype is defined by elevated blood or sputum eosinophils and is associated with FeNO, IL-5/IL-13 signaling, a possible response to inhaled corticosteroids and biologic agents. The mixed phenotype demonstrates dual neutrophilic and Th2 inflammation. Paucigranulocytic phenotypes remain poorly characterized but with distinct characteristics. Finally, dysregulation of macrophages and lymphocytes as inflammation mediators needs to be studied further. Recent advances have introduced a variety of therapeutic strategies targeting specific inflammatory pathways. Bronchiectasis has a spectrum of inflammatory phenotypes with distinct biological and clinical implications. Recognition and better understanding of inflammatory phenotypes in bronchiectasis may enable opportunities for personalized precision medicine through the transition from empirical management to biomarker-guided, personalized care.

Asthma is a complex inflammatory airway disease affecting a significant global population, spanning from childhood through adulthood. Despite advances in treatment modalities, a significant subset of patients, approximately 10%, grapple with severe asthma, characterized by increased healthcare utilization and diminished quality of life. Tezepelumab, a monoclonal antibody targeting thymic stromal lymphopoietin (TSLP), offers promising therapeutic potential. TSLP is a protein released by a variety of cells, with a predominance of epithelial cells, in reaction to plenty of stimuli, such examples as viruses, aeroallergens, and others. Its action is upstream and pertains to initiating numerous subsequent innate and adaptive immune reactions, contributing to the continuation of asthma pathophysiological processes. Tezepelumab’s unique efficacy spans diverse severe asthma phenotypes, significantly reducing exacerbation rates across eosinophilic and non-eosinophilic subtypes. Its favorable safety profile and clinically meaningful improvements in asthma control, accompanied by reductions in cytokine levels and baseline biomarkers, underscore its broad impact on asthma inflammation. Its efficacy, irrespective of type 2 (T2) endotype, reinforces the idea that TSLP blockade broadly inhibits pathways crucial to asthma pathophysiology, rather than narrowly focusing on individual downstream factors, as previous biological treatments have. This review discusses the rationale for TSLP blockade and the efficacy of tezepelumab in severe asthma using data from key trials.