Abstract
Wound healing is a multi-phased pathophysiological process requiring chemoattractant receptor-dependent accumulation of myeloid cells in the lesion. Two G protein-coupled formylpeptide receptors Fpr1 and Fpr2 mediate rapid neutrophil infiltration in the liver of Listeria-infected mice by sensing pathogen-derived chemotactic ligands. These receptors also recognize host-derived chemotactic peptides in inflammation and injury. Here we report the capacity of Fprs to promote the healing of sterile skin wound in mice by initiating neutrophil infiltration. We found that in normal miceneutrophils rapidly infiltrated the dermis in the wound before the production of neutrophil-specific chemokines by the injured tissue. In contrast, rapid neutrophil infiltration was markedly reduced with delayed wound closure in mice deficient in both Fprs. In addition, we detected Fpr ligand activity that chemoattracted neutrophils into the wound tissue. Our study thus demonstrates that Fprs are critical for normal healing of the sterile skin wound by mediating the first wave of neutrophil infiltration.
Highlights
Wound healing is an interactive process that involves soluble mediators, components of extracellular matrix, resident cells, and infiltrating leukocyte subsets
The accumulation of neutrophils is controlled by multiple chemoattractants [2,3], such as IL-8 (CXCL8), neutrophilactivating peptide-2 (NAP-2;CXCL7) [4], and growth-related oncogene a (GRO-a) (CXCL1) [5,6], which use G proteincoupled chemokine receptors (GPCRs) expressed by neutrophils
The healing of skin wound in Fpr1/2-/-mice was significantly delayed as compared with WT mice
Summary
Wound healing is an interactive process that involves soluble mediators, components of extracellular matrix, resident cells (epithelial cells, fibroblasts, endothelial cells, nerve cells), and infiltrating leukocyte subsets. We examined the role of Fpr1 and Fpr2 in the healing of full-thickness skin wound in mice by using mouse strains deficient in Fprs. A pan-Fpr antagonist, Boc-2, significantly delayed the healing of the skin wound in WT mice (Fig. 1B).
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