ArticleJournal of advanced research2026
Aryl hydrocarbon receptor impairs HK2-controlled flux of the hexosamine biosynthesis pathway to suppress NETosis in an N-glycosylation-dependent manner.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Unraveling the pleiotropic roles of the mTOR-glycolytic axis in ulcerative colitis: from immunometabolic dysregulation to mucosal barrier remodeling.Frontiers in immunology · 2026Review
- Aryl Hydrocarbon Receptor in Health and Disease.MedComm · 2025Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe aryl hydrocarbon receptor (AhR) is a promising therapeutic target for ulcerative colitis (UC) and plays a role in regulating neutrophil function.
objectiveWe aimed to investigate the effects and mechanisms of AhR on NETosis, a neutrophil-driven process that disrupts intestinal epithelial homeostasis, to support the development of anti-UC therapies.
methodsA dextran sulphate sodium (DSS)-induced colitis mouse model was established, and bioinformatics analyses combined with multiple molecular biology techniques were used to assess changes in NETosis and signalling pathway activation.
resultsData from the Gene Expression Omnibus database and DSS-induced colitis mice confirmed an inverse correlation between AhR activation and NETosis in UC. In vitro experiments, including assays for double-stranded DNA release, co-localisation of myeloperoxidase with DNA and neutrophil elastase (NE)/citrullinated histone H3, histone H4 degradation, and chromatin decondensation, demonstrated that AhR activation directly inhibits NETosis. Further investigations using gene knockdown plasmids, enzyme substrate assays, and flow cytometry revealed that AhR activation reduced the NE activity-independent of pcDNA-peptidyl arginine deiminase 4-through an N-glycosylation-dependent mechanism involving the physiological NE inhibitors alpha-1 antitrypsin (AAT) and alpha-2-macroglobulin (A2M). Mechanistically, AhR functioned as an E3 ligase that bound to hexokinase 2 (HK2), promoting its K48-linked ubiquitination and degradation, thereby impairing the flux of the hexosamine biosynthesis pathway (HBP) and reducing the availability of the glycosylation precursor UDP-GlcNAc.
conclusionAhR activation suppresses NETosis by modulating HK2-mediated HBP flux and the subsequent N-glycosylation of AAT and A2M, thereby decreasing NE activity.
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