Cited by 266Liver physiology and pathologyAutophagy in Disease and TherapyLiver Diseases and Immunity

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Macrophage autophagy protects against liver fibrosis in mice

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Lodder, Jasper, Denaës, Timothé, Chobert, Marie-Noële, Wan, JingHong, El-Benna, Jamel, Pawlotsky, Jean-Michel, Lotersztajn, Sophie, Teixeira-Clerc, Fatima·2015·Autophagy

DOI 10.1080/15548627.2015.1058473PMC PMC4590651

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Abstract

Autophagy is a lysosomal degradation pathway of cellular components that displays antiinflammatory properties in macrophages. Macrophages are critically involved in chronic liver injury by releasing mediators that promote hepatocyte apoptosis, contribute to inflammatory cell recruitment and activation of hepatic fibrogenic cells. Here, we investigated whether macrophage autophagy may protect against chronic liver injury. Experiments were performed in mice with mutations in the autophagy gene Atg5 in the myeloid lineage (Atg5(fl/fl) LysM-Cre mice, referred to as atg5(-/-)) and their wild-type (Atg5(fl/fl), referred to as WT) littermates. Liver fibrosis was induced by repeated intraperitoneal injection of carbon tetrachloride. In vitro studies were performed in cultures or co-cultures of peritoneal macrophages with hepatic myofibroblasts. As compared to WT littermates, atg5(-/-) mice exposed to chronic carbon tetrachloride administration displayed higher hepatic levels of IL1A and IL1B and enhanced inflammatory cell recruitment associated with exacerbated liver injury. In addition, atg5(-/-) mice were more susceptible to liver fibrosis, as shown by enhanced matrix and fibrogenic cell accumulation. Macrophages from atg5(-/-) mice secreted higher levels of reactive oxygen species (ROS)-induced IL1A and IL1B. Moreover, hepatic myofibroblasts exposed to the conditioned medium of macrophages from atg5(-/-) mice showed increased profibrogenic gene expression; this effect was blunted when neutralizing IL1A and IL1B in the conditioned medium of atg5(-/-) macrophages. Finally, administration of recombinant IL1RN (interleukin 1 receptor antagonist) to carbon tetrachloride-exposed atg5(-/-) mice blunted liver injury and fibrosis, identifying IL1A/B as central mediators in the deleterious effects of macrophage autophagy invalidation. These results uncover macrophage autophagy as a novel antiinflammatory pathway regulating liver fibrosis.

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Background
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Authors: Lodder, J., Denaës, T., Chobert, M.-N., Wan, J., El-Benna, J., Pawlotsky, J.-M., Lotersztajn, S., & Teixeira-Clerc, F.
Affiliations: Inserm (FR)
INSERM UMR-1149; Centre de Recherche sur l'Inflammation; Paris; France
Corresponding author: Lotersztajn, Sophie
Teixeira-Clerc, Fatima
ORCID: Lodder, Jasper
Wan, JingHong
Pawlotsky, Jean-Michel
Lotersztajn, Sophie
Teixeira-Clerc, Fatima
Venue: Autophagy
Publisher: Informa UK Limited
Published: 2015-08-03
Volume: 11
Issue: 8
Pages: 1280-1292
ISSN: 1554-8627 (ISSN-L)
1554-8635
DOI: 10.1080/15548627.2015.1058473
PMC: PMC4590651
OpenAlex: W1807054663
Cited by: 266
References: 43
Citations by year: 2026: 14 · 2025: 22 · 2024: 21 · 2023: 31 · 2022: 23 · 2021: 34 · 2020: 25 · 2019: 25 · 2018: 28 · 2017: 19 · 2016: 17 · 2015: 5
FWCI: 13.63
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Autophagy (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Agence Nationale de la Recherche (ANR-11-IDEX-0005)
Institut National de la Santé et de la Recherche Médicale (ANR-11-Idex-005-02)
Topics: Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
Keywords: macrophage autophagy, liver fibrosis, ATG5, carbon tetrachloride-induced liver injury, interleukin-1 alpha, IL-1β, interleukin-1 receptor antagonist, hepatic myofibroblasts, reactive oxygen species, chronic inflammation, anti-inflammatory pathways
MeSH terms: Autophagy-Related Protein 5, Animals, Autophagy, Carbon Tetrachloride, Disease Models, Animal, Inflammation, Kupffer Cells, Liver, Liver Cirrhosis, Lysosomes, Macrophages, Microtubule-Associated Proteins, Mutation, Neutrophils, Recombinant Proteins, Culture Media, Conditioned, Reactive Oxygen Species, Macrophages, Peritoneal, Mice, Knockout, Cell Lineage, Mice, Interleukin-1alpha, Interleukin-1beta, Myofibroblasts

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Macrophage autophagy protects against liver fibrosis in mice

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