ArticleFrontiers in medicine2025
IDO1 induced macrophage M1 polarization via ER stress-associated GRP78-XBP1 pathway to promote ulcerative colitis progression.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed.
- Targeting tryptophan metabolism in breast cancer immunotherapy: Recent advances and future prospects.Translational oncology · 2026Review
- GRP78 in viral pneumonia: dual regulatory mechanisms and translational prospects.Clinical and experimental medicine · 2026Review
- Machine learning-based identification of a metabolic cell death gene signature for assessing disease activity and immunological landscape in inflammatory bowel disease.Scientific reports · 2026Article
- Astragaloside IV Alleviates DSS-Induced Ulcerative Colitis by Modulating Host-Gut Tryptophan Metabolism.Foods (Basel, Switzerland) · 2026Article
- Article
- Metabolic characterization of tumor-immune interactions by multiplexed immunofluorescence reveals spatial mechanisms of immunotherapy response in non-small cell lung carcinoma (NSCLC).Nature communications · 2026Article
- Identification and validation of aryl hydrocarbon receptor-associated hub genes in ulcerative colitis via integrated bioinformatics analysis.Human genomics · 2025Article
- Indoximod Attenuates Inflammatory Responses in Acetic Acid-Induced Acute Colitis by Modulating Toll-like Receptor 4 (TLR4) Signaling and Proinflammatory Cytokines in Rats.Medicina (Kaunas, Lithuania) · 2025Article
- Multi-omics integration analysis based on plasma circulating proteins reveals potential therapeutic targets for ulcerative colitis.Frontiers in molecular biosciences · 2025Article
- Low Indoleamine 2,3-Dioxygenase 1 Expression Enhances Dendritic Cells Response to Tumor Cells Against Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2025Article
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6 authors.
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Abstract
Ulcerative colitis (UC) is a chronic inflammatory bowel disorder distinguished by alternating phases of remission and exacerbation. Restoring immune balance through the modulation of M1 macrophage polarization represents a potentially valuable therapeutic strategy for UC. Indoleamine 2,3-dioxygenase-1 (IDO1) has been shown to contribute to macrophage plasticity, but its role in the pathogenesis of UC via regulating M1 macrophage polarization has not been studied yet. For the clinical component, we analyzed IDO1 expression in UC using bioinformatics analysis of Gene Expression Omnibus (GEO) datasets and validated the result using western blotting of colonic tissues from new recruited UC patients. Colitis was induced in mice via dextran sulfate sodium (DSS) treatment and subsequently treated with oral administration of 1-methyl-DL-tryptophan (1-MT), an inhibitor of IDO1 pathway. The results indicated that IDO1 expression was significantly elevated in UC patients and correlated with M1 macrophage polarization observed in both human data and colitis mice. Furthermore, 1-MT markedly ameliorated DSS-induced weight loss, colonic shortening and disease severity via inhibiting IDO1 expression level, downregulating GRP78-XBP1 pathway and reducing M1 proportion. Notably,
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