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Because of its potency for expanding stem cell populations, delivery of exogenous LIF to diseased tissue could have therapeutic value. However, systemic elevations of LIF can have negative, off-target effects. We tested whether inflammatory cells expressing a LIF transgene under control of a leukocyte-specific, CD11b promoter provide a strategy to target LIF to sites of damage in the mdx mouse model of Duchenne muscular dystrophy, leading to increased numbers of muscle stem cells and improved muscle regeneration. However, transgene expression in inflammatory cells did not increase muscle growth or increase numbers of stem cells required for regeneration. Instead, transgene expression disrupted the normal dispersion of macrophages in dystrophic muscles, leading to transient increases in muscle damage in foci where macrophages were highly concentrated during early stages of pathology. The defect in inflammatory cell dispersion reflected impaired chemotaxis of macrophages to C-C motif chemokine ligand-2 and local increases of LIF production that produced large aggregations of cytolytic macrophages. Transgene expression also induced a shift in macrophage phenotype away from a CD206+, M2-biased phenotype that supports regeneration. However, at later stages of the disease when macrophage numbers declined, they dispersed in the muscle, leading to reductions in muscle fiber damage, compared to non-transgenic mdx mice. Together, the findings show that macrophage-mediated delivery of transgenic LIF exerts differential effects on macrophage dispersion and muscle damage depending on the stage of dystrophic pathology.<\/jats:p>","DOI":"10.1093\/hmg\/ddab230","type":"journal-article","created":{"date-parts":[[2021,8,6]],"date-time":"2021-08-06T19:12:21Z","timestamp":1628277141000},"page":"189-206","source":"Crossref","is-referenced-by-count":5,"title":["Myeloid cell-mediated targeting of LIF to dystrophic muscle causes transient increases in muscle fiber lesions by disrupting the recruitment and dispersion of macrophages in muscle"],"prefix":"10.1093","volume":"31","author":[{"given":"Ivan","family":"Flores","sequence":"first","affiliation":[{"name":"Molecular, Cellular & Integrative Physiology Program, University of California, Los Angeles, CA 90095-1606, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven S","family":"Welc","sequence":"additional","affiliation":[{"name":"Department of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA"},{"name":"Indiana Center for Musculoskeletal Health, Indiana University School of Medicine, Indianapolis, IN 46202, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle","family":"Wehling-Henricks","sequence":"additional","affiliation":[{"name":"Department of Integrative Biology and Physiology, University of California, Los Angeles, CA 90095-1606, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James G","family":"Tidball","sequence":"additional","affiliation":[{"name":"Molecular, Cellular & Integrative Physiology Program, University of California, Los Angeles, CA 90095-1606, USA"},{"name":"Department of Integrative Biology and Physiology, University of California, Los Angeles, CA 90095-1606, USA"},{"name":"Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, University of California, Los Angeles, CA 90095, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2021,8,14]]},"reference":[{"key":"2022010913470262700_ref1","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1038\/s41467-019-10614-1","article-title":"Targeting a therapeutic LIF transgene to muscle via the immune system ameliorates muscular dystrophy","volume":"10","author":"Welc","year":"2019","journal-title":"Nat. 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