ArticlePLoS pathogens2014
Absence of intestinal PPARγ aggravates acute infectious colitis in mice through a lipocalin-2-dependent pathway.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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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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.
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Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- Dietary conjugated linoleic acid enhances resistance toGut microbes · 2026Article
- Article
- From tissue to blood: an integrated multi-omics signature identifies fibrogenesis and neutrophil activation as key drivers of ulcerative colitis severity.Frontiers in immunology · 2026Article
- Differential Impacts of Environmentally Relevant Microplastics on Gut Barrier Integrity in Mice Fed High-Fat Diet Versus Normal Chow Diet.Metabolites · 2025Article
- Oncogenic and tumor-suppressive roles of Lipocalin 2 (LCN2) in tumor progression.Oncology research · 2025Review
- Macrophage polarization in disease therapy: insights from astragaloside IV and cycloastragenol.Frontiers in pharmacology · 2025Review
- Sodium Humate-Derived Gut Microbiota Ameliorates Intestinal Dysfunction Induced byMicrobiology spectrum · 2023Article
- Lycium barbarum polysaccharides alleviate LPS-induced inflammatory responses through PPARγ/MAPK/NF-κB pathway in bovine mammary epithelial cells.Journal of animal science · 2022Article
- A potential therapeutic target in traditional Chinese medicine for ulcerative colitis: Macrophage polarization.Frontiers in pharmacology · 2022Review
- Fecal Lcn-2 level is a sensitive biological indicator for gut dysbiosis and intestinal inflammation in multiple sclerosis.Frontiers in immunology · 2022Article
- The effect ofJournal of diabetes and metabolic disorders · 2020Article
- Peroxisome Proliferator-Activated Receptors as Molecular Links between Caloric Restriction and Circadian Rhythm.Nutrients · 2020Review
- PPARs and Microbiota in Skeletal Muscle Health and Wasting.International journal of molecular sciences · 2020Review
- Review
- Lipocalin 2 links inflammation and ankylosis in the clinical overlap of inflammatory bowel disease (IBD) and ankylosing spondylitis (AS).Arthritis research & therapy · 2020Article
- The role of lipocalin-2 in age-related macular degeneration (AMD).Cellular and molecular life sciences : CMLS · 2020Review
- Pioglitazone-Mediated Attenuation of Experimental Colitis Relies on Cleaving of Annexin A1 Released by Macrophages.Frontiers in pharmacology · 2020Article
- Gut Microbiota, Peroxisome Proliferator-Activated Receptors, and Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2020Review
- Clostridium ramosum regulates enterochromaffin cell development and serotonin release.Scientific reports · 2019Article
- Interactions between Host PPARs and Gut Microbiota in Health and Disease.International journal of molecular sciences · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To be able to colonize its host, invading Salmonella enterica serovar Typhimurium must disrupt and severely affect host-microbiome homeostasis. Here we report that S. Typhimurium induces acute infectious colitis by inhibiting peroxisome proliferator-activated receptor gamma (PPARγ) expression in intestinal epithelial cells. Interestingly, this PPARγ down-regulation by S. Typhimurium is independent of TLR-4 signaling but triggers a marked elevation of host innate immune response genes, including that encoding the antimicrobial peptide lipocalin-2 (Lcn2). Accumulation of Lcn2 stabilizes the metalloproteinase MMP-9 via extracellular binding, which further aggravates the colitis. Remarkably, when exposed to S. Typhimurium, Lcn2-null mice exhibited a drastic reduction of the colitis and remained protected even at later stages of infection. Our data suggest a mechanism in which S. Typhimurium hijacks the control of host immune response genes such as those encoding PPARγ and Lcn2 to acquire residence in a host, which by evolution has established a symbiotic relation with its microbiome community to prevent pathogen invasion.
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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.