Type 2 inflammation promotes distinct metabolic profiles in chronic rhinosinusitis with nasal polyps

Chronic rhinosinusitis (CRS) is an inflammatory disorder of the sinonasal mucosa that occurs with or without nasal polyps (NPs). Compared with CRS without NPs, CRS with NPs (CRSwNP) is associated with more severe and uncontrolled sinonasal symptoms (1). Type 2 inflammation, driven by TH2 cytokines (interleukins 4, 5, and 13), promotes eosinophilic infiltration into NPs and contributes to disease progression and recurrence (2). Although recent studies have emphasized biological phenoty-ping and identified genetic/epigenetic endotypes to optimize treatment strategies for CRSwNP (3), clinical translation remains limited. Because cellular phenotypes are strongly influenced by metabolic alterations (4), profiling of the metabolic landscape may provide insight into CRSwNP pathogenesis and identify bio-markers of type 2 inflammation-related symptom exacerbation, treatment resistance, and recurrence. However, metabolomic characterization of CRSwNP remains underexplored.