ArticleScientific reports2015
Severity of DSS-induced colitis is reduced in Ido1-deficient mice with down-regulation of TLR-MyD88-NF-kB transcriptional networks.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
62 citing papers in PubMed, 91 citations in OpenAlex.
- Sustained Diet-Induced Remission in Pediatric Crohn's Disease Is Associated With Kynurenine and Serotonin Pathways.Inflammatory bowel diseases · 2023Trial
- The gut microbiota-tryptophan metabolism-immune axis in inflammatory bowel disease: Mechanisms and therapeutic prospects.Human vaccines & immunotherapeutics · 2026Review
- Tracing NADCell reports · 2026Article
- Pre-Treatment with Estradiol, But not Progesterone, Exacerbates DSS Colitis: Dysregulated Innate Immunity and Impaired Epithelial Damage Response.Inflammation · 2026Article
- 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
- DSS Colitis Model: Traps, Tricks, and Reporting Recommendations.Biomedicines · 2026Review
- Intestinal amino acid metabolic response and its roles in inflammatory bowel disease.Cell communication and signaling : CCS · 2025Review
- Tracing NADResearch square · 2025Article
- Time- and dose-dependent activation of the NLRP3 and MyD88/NF-κB pathways by Trueperella pyogenes membrane vesicles in bovine endometrial epithelial cells.Veterinary research · 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
- Anti-Inflammatory Activity of Cell-Penetrating Peptide Nucleic Acids Targeting Indoleamine 2,3-Dioxygenase 1 in IFNγ-Treated Human Keratinocytes.Biomolecules & therapeutics · 2025Article
- Activation of PPARγ regulates M1/M2 macrophage polarization and attenuates dextran sulfate sodium salt-induced inflammatory bowel disease via the STAT-1/STAT-6 pathway.The Kaohsiung journal of medical sciences · 2025Article
- Article
- IDO1 promotes CSFV replication by mediating tryptophan metabolism to inhibit NF-κB signaling.Journal of virology · 2024Article
- Unveiling Colitis: A Journey through the Dextran Sodium Sulfate-induced Model.Inflammatory bowel diseases · 2024Review
- An immune-competent human gut microphysiological system enables inflammation-modulation by Faecalibacterium prausnitzii.NPJ biofilms and microbiomes · 2024Article
- FAM76B regulates PI3K/Akt/NF-κB-mediated M1 macrophage polarization by influencing the stability of PIK3CD mRNA.Cellular and molecular life sciences : CMLS · 2024Article
- Article
- An immune-competent human gut microphysiological system enables inflammation-modulation ofResearch square · 2023Article
- Gut taste receptor type 1 member 3 is an intrinsic regulator of Western diet-induced intestinal inflammation.BMC medicine · 2023Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Indoleamine 2,3 -dioxygenase 1 (IDO1) catalyzes L-tryptophan to kynurenine in the first and rate-limiting step of tryptophan metabolism. IDO1 is expressed widely throughout the body, with especially high expression in colonic intestinal tissues. To examine the role of IDO1 in the colon, transcriptome analysis was performed in both Ido1(-/-) and Ido1(+/+) mice. Gene set enrichment analysis identified the Inflammatory Response as the most significant category modulated by the absence of IDO1. This observation prompted us to further investigate the function of IDO1 in the development of tissue inflammation. By using DSS-induced experimental colitis mice models, we found that the disease in Ido1(-/-) mice was less severe than in Ido1(+/+) mice. Pharmacological inhibition of IDO1 by L-1MT attenuated the severity of DSS-colitis as well. Transcriptome analyses revealed that pathways involving TLR and NF-kB signaling were significantly down-regulated by the absence of IDO1. Furthermore, dramatic changes in TLR and NF-kB signaling resulted in substantial changes in the expression of many inflammatory cytokines and chemokines. Numbers of inflammatory cells in colon and peripheral blood were reduced in IDO1 deficiency. These findings suggest that IDO1 plays important roles in producing inflammatory responses and modulating transcriptional networks during the development of colitis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.