ArticlemBio2021
5-Aminosalicylic Acid Ameliorates Colitis and Checks Dysbiotic Escherichia coli Expansion by Activating PPAR-γ Signaling in the Intestinal Epithelium.
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Article in mBio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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81citing papers in PubMed
7.5field-weighted citation impact, top 2% of its field
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Who cites it
81 citing papers in PubMed, 127 citations in OpenAlex.
- Host metabolism shapes the intestinal microbiota: a top-down paradigm of environmental selection pressure.Gut microbes · 2026Review
- Thiazolidinedione Use and Risk of Bacterial Enteric Infection Among Adults With Type 2 Diabetes Mellitus.Open forum infectious diseases · 2026Article
- Norcantharidin Ameliorates Experimental Ulcerative Colitis Through Epigenetic and Metabolic Reprogramming Involving IL-6/DNMT1/SOCS3 and AMPK/SIRT1/FOXO3a-Nrf2 Signaling.International journal of molecular sciences · 2026Article
- Oxygen homeostasis: new insight of gut microbiota-host interactions.NPJ biofilms and microbiomes · 2026Review
- Restoring O-glycosylation and expression of MUC2 limits progression of colorectal cancer.Cell death & disease · 2026Article
- DsbA-L safeguards T cell mitochondrial redox homeostasis to restrain Th17 differentiation and colitis.Cell death & disease · 2026Article
- Shenling Baizhu powder reduced the oxidative stress and mitochondrial damage during ulcerative colitisthe Kelch-like ECH-associated protein 1-NF-E2-related factor 2/nuclear factor kappa B pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- EnterohemorrhagiciScience · 2026Article
- Paragonimus proliferus Metacercaria-derived antigens mitigate DSS-Induced Ulcerative Colitis via immunomodulation and gut microbiota reconfiguration.PLoS neglected tropical diseases · 2026Article
- Integrated Multi-Omics Analysis Reveals Activation of the PPAR Signaling Pathway by Koumiss in Experimental Ulcerative Colitis.International journal of molecular sciences · 2026Article
- Host-derived nitrate fuels indole production byScience (New York, N.Y.) · 2026Article
- PPAR-γ Activation Alleviates Intestinal Dysfunction and Lactose Malabsorption in Experimental Food Allergy Rats.Nutrients · 2026Article
- Ulcerative colitis: signaling pathways, therapeutic targets and interventional strategies.Signal transduction and targeted therapy · 2026Review
- pH-responsive hyaluronic acid-RSC advances · 2026Article
- Gegen Qinlian Decoction, a classic traditional Chinese medicine formula: a potential therapeutic strategy for ulcerative colitis and colorectal cancer.Frontiers in pharmacology · 2026Review
- The signaling pathway of PPAR-γ and its protective role in various diseases.Caspian journal of internal medicine · 2026Review
- Probiotic drug interactions in ulcerative colitis: a microbiota and metabolite perspective.Frontiers in microbiology · 2026Review
- Integrated Single Cell Spatial Analysis Reveals Dysregulated Basal Progenitor Cells in Ulcerative Colitis Pathogenesis: A Multi Omics Study.Health science reports · 2026Article
- Intestinal oxygen and microbiota crosstalk: implications for pathogenesis of gastrointestinal diseases and emerging therapeutic strategies.Gut pathogens · 2025Review
- Single-Cell Transcriptomics Unravels Growth Factor Erv1-Like Mediated Ferroptosis as a Key Driver of Intestinal Epithelial Dysfunction in Ulcerative Colitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Stephanie A CevallosDepartment of Medical Microbiology and Immunology, School of Medicine, University of California Davis, Davis, California, USA.
Jee-Yon LeeDepartment of Medical Microbiology and Immunology, School of Medicine, University of California Davis, Davis, California, USA.
Eric M VelazquezDepartment of Medical Microbiology and Immunology, School of Medicine, University of California Davis, Davis, California, USA.
Nora J FoegedingVanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Catherine D SheltonVanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Connor R TiffanyDepartment of Medical Microbiology and Immunology, School of Medicine, University of California Davis, Davis, California, USA.ORCID 0000-0001-8188-7720
Beau H ParryDepartment of Medical Microbiology and Immunology, School of Medicine, University of California Davis, Davis, California, USA.
Annica R Stull-LaneDepartment of Medical Microbiology and Immunology, School of Medicine, University of California Davis, Davis, California, USA.
Erin E OlsanDepartment of Medical Microbiology and Immunology, School of Medicine, University of California Davis, Davis, California, USA.
Hannah P SavageDepartment of Medical Microbiology and Immunology, School of Medicine, University of California Davis, Davis, California, USA.
Henry NguyenDepartment of Medical Microbiology and Immunology, School of Medicine, University of California Davis, Davis, California, USA.
Star S GhanaatDepartment of Medical Microbiology and Immunology, School of Medicine, University of California Davis, Davis, California, USA.
Austin J ByndlossDepartment of Medical Microbiology and Immunology, School of Medicine, University of California Davis, Davis, California, USA.
Ilechukwu O AguDepartment of Medical Microbiology and Immunology, School of Medicine, University of California Davis, Davis, California, USA.
Renée M TsolisDepartment of Medical Microbiology and Immunology, School of Medicine, University of California Davis, Davis, California, USA.ORCID 0000-0001-9131-6657
Mariana X Byndloss *Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, Tennessee, USA.ORCID 0000-0002-2122-4156
Andreas J Bäumler *Department of Medical Microbiology and Immunology, School of Medicine, University of California Davis, Davis, California, USA ajbaumler@ucdavis.edu.ORCID 0000-0001-9152-7809
University of California, Davis · USVanderbilt University Medical Center · US
Funding
Vanderbilt-Ingram Cancer Center SPORE in Gastrointestinal CancerP50CA236733 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI STEPHEN W. FESIK · 2019 to 2026
$19.6MUC Davis Clinical and Translational Science CenterUL1TR000002 · NCATS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERGLUND, LARS F · 2012 to 2015
$12.2MVirulence Factors of SalmonellaR01AI044170 · NIAID · UNIVERSITY OF CALIFORNIA DAVIS · PI BAUMLER, ANDREAS J · 1999 to 2022
$8.5MTRAINING IN GASTROENTEROLOGYT32DK007673 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 1992 to 2026
$8.4MMicrobiota Outgrowth by SalmonellaR01AI096528 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BAUMLER, ANDREAS J · 2011 to 2025
$6.1MMechanism of Colonization ResistanceR01AI112949 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Andreas J Baumler · 2016 to 2026
$5.2MInnate immune sensing of ER stress during bacterial infectionR01AI109799 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI TSOLIS, RENEE M · 2014 to 2024
$3.6MNeutrophil-intrinsic role of SLC11A1/NRAMP1 in control of bacterial infectionR01AI149632 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI TSOLIS, RENEE M · 2019 to 2023
$2.4MSalmonella Host interactionsR37AI044170 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Andreas J Baumler, Renee M Tsolis · 2025 to 2026
$1.2MUC Davis Clinical and Translational Science CenterTL1TR000133 · NCATS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERGLUND, LARS F · 2012 to 2015
$594kDietary copper reconfigures pathogen growthR21AI146432 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BAUMLER, ANDREAS J · 2019 to 2020
$432kRole of NRAMP1/SLC11A1 in Salmonella pathogenesisR21AI143253 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI TSOLIS, RENEE M · 2019 to 2020
$432kNCATS NIH HHS TL1 TR000133NCATS NIH HHS UL1 TR000002NCI NIH HHS P50 CA236733NIAID NIH HHS R01 AI044170NIAID NIH HHS R01 AI096528NIAID NIH HHS R01 AI109799NIAID NIH HHS R01 AI112949NIAID NIH HHS R01 AI149632NIAID NIH HHS R21 AI143253NIAID NIH HHS R21 AI146432NIAID NIH HHS R21 AI153069NIAID NIH HHS R37 AI044170NIAID NIH HHS R56 AI112949NIDDK NIH HHS T32 DK007673
Abstract
5-Aminosalicylic acid (5-ASA), a peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist, is a widely used first-line medication for the treatment of ulcerative colitis, but its anti-inflammatory mechanism is not fully resolved. Here, we show that 5-ASA ameliorates colitis in dextran sulfate sodium (DSS)-treated mice by activating PPAR-γ signaling in the intestinal epithelium. DSS-induced colitis was associated with a loss of epithelial hypoxia and a respiration-dependent luminal expansion of
Indexed as
AnimalsAnti-Inflammatory Agents, Non-SteroidalColitisColonCytochrome b GroupDextran SulfateDysbiosisElectron Transport Chain Complex ProteinsEscherichia coliEscherichia coli ProteinsFemaleGene Expression RegulationInflammationMaleMesalamineMiceAnti-Inflammatory Agents, Non-Steroidalcytochrome bd terminal oxidase complex, E coliCytochrome b GroupDextran SulfateElectron Transport Chain Complex ProteinsEscherichia coli ProteinsMesalamineMicrofilament ProteinsnapA protein, E coliNarG protein, E colinarZ protein, E coliNitrate ReductaseOxidoreductasesPPAR gammaPparg protein, mouseVil1 protein, mousedysbiosisEscherichia coligut inflammationinflammatory bowel diseasemicrobial communities
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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.