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Epidermal cells help coordinate leukocyte migration during inflammation through fatty acid-fueled matrix metalloproteinase production

ABSTRACT: In addition to satisfying the metabolic demands of cells, mitochondrial metabolism helps regulate immune cell function. To date, such cell-intrinsic metabolic-immunologic cross-talk has only been described operating in cells of the immune system. Here we show that epidermal cells utilize fatty acid β-oxidation to fuel their contribution to the immune response during cutaneous inflammation. By live imaging metabolic and immunological processes within intact zebrafish embryos during cutaneous inflammation, we uncover a mechanism where elevated β-oxidation-fueled mitochondria-derived reactive oxygen species within epidermal cells helps guide matrix metalloproteinase-driven leukocyte recruitment. This mechanism requires the activity of a zebrafish homolog of the mammalian mitochondrial enzyme, Immunoresponsive gene 1. This study describes the first example of metabolic reprogramming operating within a non-immune cell type to help control its contribution to the immune response. Targeting of this metabolic-immunologic interface within keratinocytes may prove useful in treating inflammatory dermatoses. In this study, Affymetrix Zebrafish Genome Arrays were used to identify zebrafish Irg1l (a homolog of mammalian IRG1) as a gene up-regulated in response to Salmonella infection.

ORGANISM(S): Danio rerio

PROVIDER: GSE56365 | GEO | 2014/04/01

SECONDARY ACCESSION(S): PRJNA243056

REPOSITORIES: GEO

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Epidermal cells help coordinate leukocyte migration during inflammation through fatty acid-fueled matrix metalloproteinase production

Project description:In addition to satisfying the metabolic demands of cells, mitochondrial metabolism helps regulate immune cell function. To date, such cell-intrinsic metabolic-immunologic cross-talk has only been described operating in cells of the immune system. Here we show that epidermal cells utilize fatty acid β-oxidation to fuel their contribution to the immune response during cutaneous inflammation. By live imaging metabolic and immunological processes within intact zebrafish embryos during cutaneous inflammation, we uncover a mechanism where elevated β-oxidation-fueled mitochondria-derived reactive oxygen species within epidermal cells helps guide matrix metalloproteinase-driven leukocyte recruitment. This mechanism requires the activity of a zebrafish homolog of the mammalian mitochondrial enzyme, Immunoresponsive gene 1. This study describes the first example of metabolic reprogramming operating within a non-immune cell type to help control its contribution to the immune response. Targeting of this metabolic-immunologic interface within keratinocytes may prove useful in treating inflammatory dermatoses. In this study, Affymetrix Zebrafish Genome Arrays were used to identify zebrafish Irg1l (a homolog of mammalian IRG1) as a gene up-regulated in response to Salmonella infection. The microarray analysis compared 4 day post fertilisation (dpf) dissected larval zebrafish trunks (approximately 50) that had been injected at 2 dpf with either: (i) PBS (as a negative control) or (ii) live Salmonella enterica serovar Typhimurium bacteria. The study was performed in triplicate.

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A low-complexity domain of Tet3 dioxygenase shields the oocyte methylome from oxidative erosion [ ACE-seq]

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An auto-suppression mechanism for Tet dioxygenase protects the mouse genome from oxidative demethylation

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Cutaneous arsenical exposure induces distinct metabolic transcriptional alterations of kidney cells

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