Cited by 48Inflammatory Bowel DiseaseInflammatory mediators and NSAID effectsGastrointestinal motility and disorders

The arachidonic acid metabolite 11β-ProstaglandinF2α controls intestinal epithelial healing: deficiency in patients with Crohn’s disease

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Coquenlorge, Sabrina, Van Landeghem, Laurianne, Jaulin, Julie, Cenac, Nicolas, Vergnolle, Nathalie, Duchalais, Emilie, Neunlist, Michel, Rolli-Derkinderen, Malvyne·2016·Scientific Reports

Abstract

In healthy gut enteric glial cells (EGC) are essential to intestinal epithelial barrier (IEB) functions. In Crohn’s Disease (CD), both EGC phenotype and IEB functions are altered, but putative involvement of EGC in CD pathogenesis remains unknown and study of human EGC are lacking. EGC isolated from CD and control patients showed similar expression of glial markers and EGC-derived soluble factors (IL6, TGF-β, proEGF, GSH) but CD EGC failed to increase IEB resistance and healing. Lipid profiling showed that CD EGC produced decreased amounts of 15-HETE, 18-HEPE, 15dPGJ 2 and 11βPGF 2 α as compared to healthy EGC. They also had reduced expression of the L-PGDS and AKR1C3 enzymes. Produced by healthy EGC, the 11βPGF 2 activated PPARγ receptor of intestinal epithelial cells to induce cell spreading and IEB wound repair. In addition to this novel healing mechanism our data show that CD EGC presented impaired ability to promote IEB functions through defect in L-PGDS-AKR1C3-11βPGF 2 α dependent pathway.

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  • 11-β-PGF2α is the principal immediate metabolic product of both PGD2 and PGE2.

    “11-β-PGF 2α is the principal immediate metabolic product of both PGD 2 and PGE 2 [72][73][74].”

    From Diagnosis of mast cell activation syndrome: a global "consensus-2" (2021) · cites this paper as [73]

    The Discussion (page not provided) calls 11βPGF2α the primary plasma metabolite of PGD2 and states that AKR1C3 converts PGD2 to 11βPGF2α. It does not identify 11βPGF2α as a metabolite of PGE2; its discussion of PGE2 concerns glial production and neuronal responses. (LLM, conf=0.89)

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Authors
Coquenlorge, S., Van Landeghem, L., Jaulin, J., Cenac, N., Vergnolle, N., Duchalais, E., Neunlist, M., & Rolli-Derkinderen, M.
Affiliations
  • Inserm (FR)
  • Centre National de la Recherche Scientifique (FR)
Venue
Scientific Reports
Published
2016-05-03
Volume
6
Issue
1
Pages
25203-25203
ISSN
2045-2322 (ISSN-L)
OpenAlex
W2345694465
Cited by
48
References
73
Citations by year
2026: 3 · 2025: 4 · 2024: 5 · 2023: 8 · 2022: 5 · 2021: 6 · 2020: 6 · 2019: 3 · 2018: 6 · 2017: 1 · 2016: 1
FWCI
2.96
Type
journal article
Language
en
Open access
Locations
  • Scientific Reports (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • HAL (submittedVersion, other-oa)
Funders
  • Institut National de la Santé et de la Recherche Médicale
  • Ligue Contre le Cancer
  • Centre National de la Recherche Scientifique
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
  • Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
  • Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
Keywords
arachidonic acid metabolites, enteric glial cells, intestinal epithelial barrier, Crohn's disease, lipidomics, 15-hydroxyeicosatetraenoic acid, lipocalin-type prostaglandin D synthase, AKR1C3, PPARγ, wound healing
MeSH terms
Aldo-Keto Reductase Family 1 Member C3, Adolescent, Adult, Aged, Aged, 80 and over, Cells, Cultured, Crohn Disease, Epithelial Cells, Female, Humans, Hydroxyeicosatetraenoic Acids, Intestinal Mucosa, Intestines, Male, Middle Aged, Wound Healing, Eicosapentaenoic Acid, Prostaglandin D2, Dinoprost, Coculture Techniques, Caco-2 Cells, Young Adult

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