Cited by 299Muscle Physiology and DisordersNeurogenetic and Muscular Disorders ResearchInflammatory Myopathies and Dermatomyositis

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Interleukin-10 reduces the pathology of mdx muscular dystrophy by deactivating M1 macrophages and modulating macrophage phenotype

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Villalta, S. A., Rinaldi, C., Deng, B., Liu, G., Fedor, B., Tidball, J. G.·2011·Human Molecular Genetics

DOI 10.1093/hmg/ddq523PMC PMC3024048

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Abstract

M1 macrophages play a major role in worsening muscle injury in the mdx mouse model of Duchenne muscular dystrophy. However, mdx muscle also contains M2c macrophages that can promote tissue repair, indicating that factors regulating the balance between M1 and M2c phenotypes could influence the severity of the disease. Because interleukin-10 (IL-10) modulates macrophage activation in vitro and its expression is elevated in mdx muscles, we tested whether IL-10 influenced the macrophage phenotype in mdx muscle and whether changes in IL-10 expression affected the pathology of muscular dystrophy. Ablation of IL-10 expression in mdx mice increased muscle damage in vivo and reduced mouse strength. Treating mdx muscle macrophages with IL-10 reduced activation of the M1 phenotype, assessed by iNOS expression, and macrophages from IL-10 null mutant mice were more cytolytic than macrophages isolated from wild-type mice. Our data also showed that muscle cells in mdx muscle expressed the IL-10 receptor, suggesting that IL-10 could have direct effects on muscle cells. We assayed whether ablation of IL-10 in mdx mice affected satellite cell numbers, using Pax7 expression as an index, but found no effect. However, IL-10 mutation significantly increased myogenin expression in vivo during the acute and the regenerative phase of mdx pathology. Together, the results show that IL-10 plays a significant regulatory role in muscular dystrophy that may be caused by reducing M1 macrophage activation and cytotoxicity, increasing M2c macrophage activation and modulating muscle differentiation.

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Authors: Villalta, S. A., Rinaldi, C., Deng, B., Liu, G., Fedor, B., & Tidball, J. G.
Affiliations: University of California, Los Angeles (US)
Corresponding author: Tidball, J. G.
ORCID: Villalta, S. A.
Rinaldi, C.
Deng, B.
Tidball, J. G.
Venue: Human Molecular Genetics
Publisher: Oxford University Press (OUP)
Published: 2010-11-30
Volume: 20
Issue: 4
Pages: 790-805
ISSN: 0964-6906 (ISSN-L)
1460-2083
DOI: 10.1093/hmg/ddq523
PMC: PMC3024048
OpenAlex: W2149152441
Cited by: 299
References: 67
Citations by year: 2026: 10 · 2025: 19 · 2024: 11 · 2023: 13 · 2022: 18 · 2021: 20 · 2020: 14 · 2019: 26 · 2018: 25 · 2017: 25 · 2016: 16 · 2015: 24 · 2014: 23 · 2013: 21 · 2012: 21
FWCI: 7.17
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Human Molecular Genetics (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Muscular Dystrophy Association (157881)
National Institutes of Health (5r01ar040343-12, AR40343)
National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01 AR47721, R01 AR 40343, R01AR047721, F31AR054724)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
Health Sciences › Medicine › Genetics (clinical) › Neurogenetic and Muscular Disorders Research
Health Sciences › Medicine › Rheumatology › Inflammatory Myopathies and Dermatomyositis
Keywords: IL-10, Duchenne muscular dystrophy, mdx mice, M1 macrophages, M2c macrophages, macrophage polarization, muscle damage, inducible nitric oxide synthase, macrophage cytotoxicity, IL-10 receptor, satellite cells, Pax7, myogenin, muscle regeneration, myogenesis
MeSH terms: Animals, Cell Differentiation, Cell Line, Macrophage Activation, Macrophages, Mice, Inbred C57BL, Phagocytosis, Phenotype, Regeneration, Interleukin-10, Mice, Inbred mdx, Muscle, Skeletal, Muscular Dystrophy, Duchenne, Mice, Receptors, Interleukin-10

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Interleukin-10 reduces the pathology of mdx muscular dystrophy by deactivating M1 macrophages and modulating macrophage phenotype

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