The following is a summary of “Lower serum 15-HETE level predicts nasal ILC2 accumulation during COX-1 inhibition in AERD,” published in the November 2023 issue of Allergy & Immunology by Badrani, et al.
Aspirin-exacerbated respiratory disease (AERD) is characterized by elevated levels of cysteinyl leukotrienes, prostaglandin D2, and diminished prostaglandin E2. The potential predictive value of 15-hydroxyeicosatetraenoic acid (15-HETE) in aspirin desensitization outcomes has been identified. While the accumulation of nasal group 2 innate lymphoid cells (ILC2s) during COX-1 inhibition in AERD has been established, the interplay between tissue ILC2 accumulation, reaction symptom severity, and novel lipid biomarkers remains unexplored. For a study, researchers sought to investigate whether novel lipid mediators could predict nasal ILC2 accumulation and symptom scores during COX-1 inhibitor challenges in patients with AERD.
Eight patients undergoing aspirin desensitization for AERD were included. Blood and nasal scraping samples were collected at baseline and during COX-1 inhibitor reactions, processed for flow cytometry to assess nasal ILC2s, and subjected to serum lipidomic analysis.
Among 161 tested eicosanoids, 42 serum mediators were detected. Baseline levels of 15-HETE were inversely correlated with changes in airway ILC2 numbers (r = –0.6667; P = .0428). Additionally, the cytochrome P pathway metabolite 19,20-dihydroxy-4Z,7Z,10Z,13Z,16Z-docosapentaenoic acid (19,20-diHDPA) exhibited positive correlations with changes in airway ILC2s (r = 0.7143; P = .0305) and clinical symptom scores (r = 0.5000; P = .0081).
Lower baseline levels of 15-HETE predicted increased airway ILC2 accumulation during COX-1 inhibition in AERD patients. Moreover, elevated cytochrome P pathway metabolite levels 19,20-diHDPA were associated with heightened symptoms and nasal ILC2 accumulation. Further investigations into the regulatory role of these mediators on ILC2s may enhance the understanding of AERD pathogenesis.
Source: jacionline.org/article/S0091-6749(23)00976-4/fulltext
