ArticleMediators of inflammation2014
Antagonizing arachidonic acid-derived eicosanoids reduces inflammatory Th17 and Th1 cell-mediated inflammation and colitis severity.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 37 citations in OpenAlex.
- Multi-omics atlas of the bovine coronavirus-infected calf jejunum: reduction of Phocaeicola coprophilus and deoxycholic acid linked to Th17/Treg imbalance.NPJ biofilms and microbiomes · 2026Article
- Regulating arachidonic acid metabolism: a novel strategy to prevent colorectal inflammatory cancer transformation.Journal of Cancer · 2025Review
- Effects ofFrontiers in microbiology · 2025Article
- Baicalin alleviates intestinal inflammation and microbial disturbances by regulating Th17/Treg balance and enhancing Lactobacillus colonization in piglets.Journal of animal science and biotechnology · 2024Article
- The FADS1 genotypes modify the effect of linoleic acid-enriched diet on adipose tissue inflammation via pro-inflammatory eicosanoid metabolism.European journal of nutrition · 2022Article
- Decreased Tissue Omega-6/Omega-3 Fatty Acid Ratio Prevents Chemotherapy-Induced Gastrointestinal Toxicity Associated with Alterations of Gut Microbiome.International journal of molecular sciences · 2022Article
- Fatty acid-binding protein 3 controls contact hypersensitivity through regulating skin dermal Vγ4Allergy · 2021Article
- Regulation of Intestinal Inflammation by Soybean and Soy-Derived Compounds.Foods (Basel, Switzerland) · 2021Review
- Seminal Plasma Lipidomics Profiling to Identify Signatures of Kallmann Syndrome.Frontiers in endocrinology · 2021Article
- Metabolomic alterations associated with Kallmann syndrome.Annals of translational medicine · 2020Article
- Emerging roles of metabolites of ω3 and ω6 essential fatty acids in the control of intestinal inflammation.International immunology · 2019Review
- Genome-wide association study of endo-parasite phenotypes using imputed whole-genome sequence data in dairy and beef cattle.Genetics, selection, evolution : GSE · 2019Article
- Prostaglandin-cytokine crosstalk in chronic inflammation.British journal of pharmacology · 2019Review
- The Role of Long-Chain Fatty Acids in Inflammatory Bowel Disease.Mediators of inflammation · 2019Review
- Metabolomic alterations associated with Behçet's disease.Arthritis research & therapy · 2018Article
- Dietary n-3 PUFA May Attenuate Experimental Colitis.Mediators of inflammation · 2018Article
- Remodelling of primary human CD4+ T cell plasma membrane order by n-3 PUFA.The British journal of nutrition · 2018Article
- S1000A12, Chitotriosidase, and Resolvin D1 as Potential Biomarkers of Familial Mediterranean Fever.Journal of Korean medical science · 2015Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
During colitis, activation of two inflammatory T cell subsets, Th17 and Th1 cells, promotes ongoing intestinal inflammatory responses. n-6 polyunsaturated fatty acid- (PUFA-) derived eicosanoids, such as prostaglandin E2 (PGE2), promote Th17 cell-mediated inflammation, while n-3 PUFA antagonize both Th17 and Th1 cells and suppress PGE2 levels. We utilized two genetic mouse models, which differentially antagonize PGE2 levels, to examine the effect on Th17 cells and disease outcomes in trinitrobenzene sulfonic acid- (TNBS-) induced colitis. Fat-1 mice contain the ω3 desaturase gene from C. elegans and synthesize n-3 PUFA de novo, thereby reducing the biosynthesis of n-6 PUFA-derived eicosanoids. In contrast, Fads1 Null mice contain a disrupted Δ5 desaturase gene and produce lower levels of n-6 PUFA-derived eicosanoids. Compared to Wt littermates, Fat-1 and Fads1 Null mice exhibited a similar colitic phenotype characterized by reduced colonic mucosal inflammatory eicosanoid levels and mRNA expression of Th17 cell markers (IL-17A, RORγτ, and IL-23), decreased percentages of Th17 cells and, improved colon injury scores (P ≤ 0.05). Thus, during colitis, similar outcomes were obtained in two genetically distinct models, both of which antagonize PGE2 levels via different mechanisms. Our data highlight the critical impact of n-6 PUFA-derived eicosanoids in the promotion of Th17 cell-mediated colonic inflammation.
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