PUBLICATION
Epidermal cells help coordinate leukocyte migration during inflammation through fatty acid-fuelled matrix metalloproteinase production
- Authors
- Hall, C.J., Boyle, R.H., Sun, X., Wicker, S.M., Misa, J.P., Krissansen, G.W., Print, C.G., Crosier, K.E., Crosier, P.S.
- ID
- ZDB-PUB-140524-8
- Date
- 2014
- Source
- Nature communications 5: 3880 (Journal)
- Registered Authors
- Crosier, Kathy, Hall, Chris
- Keywords
- none
- Datasets
- GEO:GSE56365
- MeSH Terms
-
- Animals
- Cell Movement*
- Dermatitis, Atopic/pathology
- Disease Models, Animal
- Epidermis/pathology*
- Fatty Acids/metabolism*
- Gene Expression Profiling
- Glucocorticoids/metabolism
- Inflammation/pathology*
- Larva/microbiology
- Leukocytes/pathology*
- Macrophages/metabolism
- Matrix Metalloproteinase 9/metabolism*
- Mice
- Mitochondria/drug effects
- Mitochondria/metabolism
- Morpholinos/pharmacology
- Neutrophil Infiltration/drug effects
- Oxidation-Reduction
- RNA, Messenger/genetics
- RNA, Messenger/metabolism
- Reactive Oxygen Species
- Receptors, Glucocorticoid/metabolism
- Salmonella Infections, Animal/metabolism
- Signal Transduction
- Survival Analysis
- Zebrafish/embryology
- Zebrafish/genetics
- Zebrafish Proteins
- PubMed
- 24852213 Full text @ Nat. Commun.
Citation
Hall, C.J., Boyle, R.H., Sun, X., Wicker, S.M., Misa, J.P., Krissansen, G.W., Print, C.G., Crosier, K.E., Crosier, P.S. (2014) Epidermal cells help coordinate leukocyte migration during inflammation through fatty acid-fuelled matrix metalloproteinase production. Nature communications. 5:3880.
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 &beta-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-fuelled mitochondria-derived reactive oxygen species within epidermal cells helps guide matrix metalloproteinase-driven leukocyte recruitment. This mechanism requires the activity of a zebrafish homologue 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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping