Inflammatory Endotypes of Chronic Rhinosinusitis and Impacts on Comorbid Asthma

Chronic rhinosinusitis (CRS) and asthma frequently coexist and are increasingly understood as manifestations of a shared "united airway" inflammatory process. However, clinical heterogeneity remains substantial, and conventional phenotyping alone does not reliably predict disease trajectory or treatment response across the upper and lower airways. Endotype-based classification, particularly differentiation of type 2 and non-type 2 inflammation, offers a framework that can refine prognostication and support more individualized management. This review synthesizes current evidence linking CRS inflammatory endotypes with asthma severity, exacerbation risk, and postoperative or medical outcomes. We summarize practical biomarkers used in routine care and research settings and discuss how these markers inform therapeutic decisions in CRS with comorbid asthma. In type 2 disease, endotype and biomarker profiles can support a more individualized treatment approach, while also informing escalation pathways in patients with persistent symptoms or recurrence, including consideration of biologic therapy in carefully selected cases. We also highlight limitations of current approaches, including overlap between inflammatory patterns, variability between tissue and systemic biomarkers, and the still-evolving definition of non-type 2 CRS, all of which can limit precision medicine in routine clinical decision-making. Future priorities include standardization of endotype definitions, validation of pragmatic biomarker panels, and integrated multidisciplinary pathways that align upper- and lower-airway outcomes. A biology-informed stratification approach may ultimately enable better patient selection for surgery, corticosteroid strategies, and biologics, improving long-term control of both CRS and asthma.