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Our aim was to characterize cellular events leading to the alteration of macrophage properties and to modulate macrophage inflammatory status using the gaseous mediator hydrogen sulfide (H2S). Using co-culture experiments, we first showed that myofibers derived from mdx mice strongly skewed the polarization of resting macrophages towards a pro-inflammatory phenotype. Treatment of mdx mice with NaHS, an H2S donor, reduced the number of pro-inflammatory macrophages in skeletal muscle, which was associated with a decreased number of nuclei per fiber, as well as reduced myofiber branching and fibrosis. Finally, we established the metabolic sensor AMP-activated protein kinase (AMPK) as a critical NaHS target in muscle macrophages. These results identify an interplay between myofibers and macrophages where dystrophic myofibers contribute to the maintenance of a highly inflammatory environment sustaining a pro-inflammatory macrophage status, which in turn favors myofiber damage, myofiber branching and establishment of fibrosis. Our results also highlight the use of H2S donors as a potential therapeutic strategy to improve the dystrophic muscle phenotype by dampening chronic inflammation.<\/jats:p>\n               <jats:p>This article has an associated First Person interview with the first author of the paper.<\/jats:p>","DOI":"10.1242\/jcs.258429","type":"journal-article","created":{"date-parts":[[2021,9,2]],"date-time":"2021-09-02T08:55:37Z","timestamp":1630572937000},"source":"Crossref","is-referenced-by-count":28,"title":["Interplay between myofibers and pro-inflammatory macrophages controls muscle damage in <i>mdx<\/i> mice"],"prefix":"10.1242","volume":"134","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5194-682X","authenticated-orcid":false,"given":"Marielle","family":"Saclier","sequence":"first","affiliation":[{"name":"Department of Biosciences, University of Milan, 20133 Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sabrina","family":"Ben Larbi","sequence":"additional","affiliation":[{"name":"Institut NeuroMyoG\u00e8ne, Universit\u00e9 Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U1217, Universit\u00e9 de Lyon, 69008 Lyon, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ha","family":"My Ly","sequence":"additional","affiliation":[{"name":"Institut NeuroMyoG\u00e8ne, Universit\u00e9 Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U1217, Universit\u00e9 de Lyon, 69008 Lyon, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eug\u00e9nie","family":"Moulin","sequence":"additional","affiliation":[{"name":"Institut NeuroMyoG\u00e8ne, Universit\u00e9 Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U1217, Universit\u00e9 de Lyon, 69008 Lyon, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3464-3322","authenticated-orcid":false,"given":"R\u00e9mi","family":"Mounier","sequence":"additional","affiliation":[{"name":"Institut NeuroMyoG\u00e8ne, Universit\u00e9 Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U1217, Universit\u00e9 de Lyon, 69008 Lyon, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1262-502X","authenticated-orcid":false,"given":"B\u00e9n\u00e9dicte","family":"Chazaud","sequence":"additional","affiliation":[{"name":"Institut NeuroMyoG\u00e8ne, Universit\u00e9 Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U1217, Universit\u00e9 de Lyon, 69008 Lyon, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5845-9223","authenticated-orcid":false,"given":"Ga\u00ebtan","family":"Juban","sequence":"additional","affiliation":[{"name":"Institut NeuroMyoG\u00e8ne, Universit\u00e9 Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U1217, Universit\u00e9 de Lyon, 69008 Lyon, France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","published-online":{"date-parts":[[2021,9,15]]},"reference":[{"key":"2021091509371184000_JCS258429C1","doi-asserted-by":"publisher","first-page":"889","DOI":"10.1172\/JCI30556","article-title":"Interplay of IKK\/NF-kappaB signaling in macrophages and myofibers promotes muscle degeneration in Duchenne muscular dystrophy","volume":"117","author":"Acharyya","year":"2007","journal-title":"J. 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