Commensal microbiota is hepatoprotective and prevents liver fibrosis in mice
Open accessAbstract
Translocation of bacteria and their products across the intestinal barrier is common in patients with liver disease, and there is evidence that experimental liver fibrosis depends on bacterial translocation. The purpose of our study was to investigate liver fibrosis in conventional and germ‐free (GF) C57BL/6 mice. Chronic liver injury was induced by administration of thioacetamide (TAA) in the drinking water for 21 wk or by repeated intraperitoneal injections of carbon tetrachloride (CCl 4 ). Increased liver fibrosis was observed in GF mice compared with conventional mice. Hepatocytes showed more toxin‐induced oxidative stress and cell death. This was accompanied by increased activation of hepatic stellate cells, but hepatic mediators of inflammation were not significantly different. Similarly, a genetic model using Myd88/Trif‐deficient mice, which lack downstream innate immunity signaling, had more severe fibrosis than wild‐type mice. Isolated Myd88/Trif‐deficient hepatocytes were more susceptible to toxin‐induced cell death in culture. In conclusion, the commensal microbiota prevents fibrosis upon chronic liver injury in mice. This is the first study describing a beneficial role of the commensal microbiota in maintaining liver homeostasis and preventing liver fibrosis.—Mazagova, M., Wang, L., Anfora, A. T., Wissmueller, M., Lesley, S. A., Miyamoto, Y., Eckmann, L., Dhungana, S., Pathmasiri, W., Sumner, S., Westwater, C., Brenner, D. A., Schnabl, B., Commensal microbiota is hepatoprotective and prevents liver fibrosis in mice. FASEB J. 29, 1043–1055 (2015). www.fasebj.org
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Pentraxin 2 (PTX2) has demonstrated anti-inflammatory and anti-fibrotic properties in multiple preclinical fibrosis models.
“pentraxin 2 (PTX2), also known as serum amyloid protein 2, has demonstrated anti-inflammatory and anti-fibrotic properties in multiple preclinical fibrosis models172,173”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [173]
Total elimination of intestinal microbiome in germ-free mice aggravates liver injury in mouse models of liver fibrosis and PSC.
“total elimination of intestinal microbiome in germ-free mice has been shown to aggravate liver injury in mouse models of liver fibrosis and PSC.64 65”
From Novel therapeutic targets for cholestatic and fatty liver disease (2022) · cites this paper as [64]
The endogenous commensal microbiota provides hepatoprotective signals; complete absence of the gut microbiota increases liver injury, probably through lack of TLR4-mediated anti-apoptotic NF-κB signalling, and increases liver fibrosis.
“It has become apparent that the endogenous commensal microbiota provides hepatoprotective signals and that complete absence of the gut microbiota results in increased liver injury — probably owing to an absence of TLR4-mediated activation of anti-apoptotic NF-κB signalling — and a subsequent increase in liver fibrosis, as demonstrated in several models13,75,76.”
From The gut microbiome and liver cancer: mechanisms and clinical translation (2017) · cites this paper as [75]
Germ-free mice show increased liver fibrosis, which seemingly contradicts the decreased fibrosis seen in gut-sterilized mice.
“However, recent studies have demonstrated an increase in liver fibrosis in germ-free mice75,76, which seemingly contradicts the decrease of liver fibrosis seen in gut-sterilized mice.”
From The gut microbiome and liver cancer: mechanisms and clinical translation (2017) · cites this paper as [75]
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“However, the more severe phenotype observed in our GF animals is congruent with recent observations demonstrating more severe hepatic injury, including fibrosis, in GF C57BL/6 mice treated with the hepatotoxins, carbon tetrachloride or thioacetamide.(39) Intriguingly, in this same study, a similar severe phenotype was…”
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- Authors
- Mazagova, M., Wang, L., Anfora, A. T., Wissmueller, M., Lesley, S. A., Miyamoto, Y., Eckmann, L., Dhungana, S., Pathmasiri, W., Sumner, S., Westwater, C., Brenner, D. A., & Scmiabl, B.
- Affiliations
- University of California San Diego (US)
- Genomics Institute of the Novartis Research Foundation (US)
- RTI International (US)
- Medical University of South Carolina (US)
- Corresponding author
- Scmiabl, Bernd
- ORCID
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2014-12-02
- Volume
- 29
- Issue
- 3
- Pages
- 1043-1055
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- PMC
- PMC4422368
- OpenAlex
- W2023380764
- Cited by
- 199
- References
- 66
- Citations by year
- 2026: 13 · 2025: 10 · 2024: 17 · 2023: 15 · 2022: 25 · 2021: 22 · 2020: 22 · 2019: 20 · 2018: 10 · 2017: 11 · 2016: 15 · 2015: 18
- FWCI
- 8.18
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The FASEB Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (K08‐DK081830, R01‐AA020703, U01‐AA021856, 2P42‐ES010337)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Keywords
- commensal microbiota, gut microbiota, liver fibrosis, hepatoprotection, germ-free mice, bacterial translocation, thioacetamide-induced liver injury, carbon tetrachloride, hepatic stellate cell activation, oxidative stress, hepatocyte death, innate immunity, intestinal barrier, chronic liver injury
- MeSH terms
- Animals, Cells, Cultured, Chromatography, Liquid, Disease Models, Animal, Humans, Immunoenzyme Techniques, Inflammation, Liver Cirrhosis, Male, Mice, Inbred C57BL, RNA, Messenger, Thioacetamide, Blotting, Western, Signal Transduction, Apoptosis, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization, Protective Agents, Reverse Transcriptase Polymerase Chain Reaction, Hepatocytes, Cell Proliferation, Mice, Real-Time Polymerase Chain Reaction, Microbiota
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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