ArticleEBioMedicine2020
Enhanced O-linked Glcnacylation in Crohn's disease promotes intestinal inflammation.
Article in EBioMedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Targeting cell death in Crohn's disease: from mechanisms to medicines.Cell death discovery · 2026Review
- Intestinal Mucin Glycosylation: Structural Regulation, Homeostasis Maintenance and Disease Association.Biomolecules · 2025Review
- O‑GlcNAcylation as an emerging molecular target for cholangiocarcinoma therapy (Review).Oncology reports · 2025Review
- Role of O-linked N-acetylglucosamine protein modification in oxidative stress-induced autophagy: a novel target for bone remodeling.Cell communication and signaling : CCS · 2024Review
- Identification of O-glycosylation related genes and subtypes in ulcerative colitis based on machine learning.PloS one · 2024Article
- The role of O-GlcNAcylation in innate immunity and inflammation.Journal of molecular cell biology · 2023Review
- Cytosolic O-GlcNAcylation and PNG1 maintain Drosophila gut homeostasis by regulating proliferation and apoptosis.PLoS genetics · 2022Article
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- O-GlcNAcylation and Its Role in Cancer-Associated Inflammation.Frontiers in immunology · 2022Review
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- Article
- Traditional herbal formula Wu-Mei-Wan alleviates TNBS-induced colitis in mice by inhibiting necroptosis through increasing RIPK3 O-GlcNAcylation.Chinese medicine · 2021Article
- Neu3 neuraminidase induction triggers intestinal inflammation and colitis in a model of recurrent human food-poisoning.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Adherent-InvasiveInternational journal of molecular sciences · 2020Review
- When Adherent-invasive E. coli plays with host glycosylation: Does it open new perspectives for therapeutic strategies in Crohn's disease?EBioMedicine · 2020Article
- Post-Translational Modifications of Transcription Factors Harnessing the Etiology and Pathophysiology in Colonic Diseases.International journal of molecular sciences · 2020Review
- DefectiveGut microbesArticle
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTreatment of Crohn's disease (CD) remains to be a challenge due to limited insights for its pathogenesis. We aimed to determine the role of O-Linked β-N-acetylglucosamine (O-GlcNAc) in the development of CD and evaluate therapeutic effects of O-GlcNAc inhibitors on CD.
methodsO-GlcNAc in intestinal epithelial tissues of CD, adherent-invasive Escherichia coli (AIEC) LF82-infected cells and mice was determined by immunoblot and immunohistochemistry. AIEC LF82 and dextran sulfate sodium were administrated into C57BL/6 mice for estabolishing inflammatory bowel disease model and for therapeutic study.
findingsO-GlcNAc was increased in intestinal epithelial tissues of CD patients and AIEC LF82-infected mice. Infection of AIEC LF82 up-regulated the level of UDP-GlcNAc and increased O-GlcNAc in human colon epithelial HCT116 and HT-29 cells. We identified that IKKβ and NF-κB were O-Glycosylated in AIEC LF82-treated cells. Mutations of IKKβ (S733A) and p65 (T352A) abrogated the O-GlcNAc in IKKβ and NF-κB and inhibited AIEC LF82-induced activation of NF-κB. Application of 6-diazO-5-oxO-L-norleucine, an agent that blocks the production of UDP-GlcNAc and inhibits O-GlcNAc, inactivated NF-κB in AIEC LF82-infected cells, enhanced the formation of autophagy, promoted the removal of cell-associated AIEC LF82, alleviated intestinal epithelial inflammation, and improved the survival of the colitis mice.
interpretationIntestinal inflammation in CD is associated with increased O-GlcNAc modification, which is required for NF-κB activation and suppression of autophagy. Targeting O-GlcNAc could be an effective therapy for inflammatory bowel disease.
fundingNational Natural Science Foundation of China (Nos. 81573087 and 81772924) and International Cooperation Foundation of Jilin Province (20190701006GH).
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