ArticleThe journal of allergy and clinical immunology. Global2026
ALOX15-driven ω-6 fatty acid metabolism promotes type 2 inflammation in eosinophilic chronic rhinosinusitis with nasal polyps.
Article in The journal of allergy and clinical immunology. Global, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Local lipid metabolism contributes to immune homeostasis in the nasal mucosa and the pathogenesis of chronic rhinosinusitis. However, lipid mediator networks underlying eosinophilic chronic rhinosinusitis (ECRS) remain poorly defined. Objective: To characterize fatty acid-derived lipid mediator profiles in nasal polyps (NPs) from patients with and without ECRS and identify pathways associated with eosinophilic inflammation. Methods: Lipidomic profiling was performed using LC-MS/MS on NP tissues from patients with ECRS (n = 4) and without ECRS (n = 4). A total of 158 ω-6 and ω-3 fatty acid-derived lipid mediators were quantified. Arachidonate 15-lipoxygenase (ALOX15) pathway activity was evaluated by quantitative PCR and ELISA. Results: ECRS NPs displayed a distinct lipidomic signature compared with non-ECRS NPs. ECRS NPs exhibited increased levels of proinflammatory ω-6 fatty acid metabolites, including 15-hydroxyeicosatetraenoic acid (15-HETE) and 13-hydroxyoctadecadienoic acid, along with elevated ALOX15 pathway products and higher ALOX15 mRNA expression. Anti-inflammatory specialized proresolving mediators, such as lipoxin A4, were also elevated within the ω-6 pathway, and lipoxin A4 levels correlated with 15-HETE levels. These patterns indicate the concurrent activation of pro- and anti-inflammatory pathways, with a predominance of ALOX15-driven ω-6 metabolites in ECRS. In contrast, the ω-3 fatty acid pathway showed only modest increases in 14,15-DiHETE and resolvin D2, suggesting a limited compensatory resolution response compared with the robust ALOX15-dependent ω-6 activity. Conclusions: ECRS NPs exhibit a skewed lipid mediator profile characterized by enhanced ALOX15-dependent ω-6 metabolism and insufficient resolution activity. This imbalance may underlie persistent type 2 inflammation in ECRS and suggests that targeting the 15-lipoxygenase pathway may offer therapeutic benefits.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.