title: Deficiency of CX3CR1 delays burn wound healing and is associated with reduced myeloid cell recruitment and decreased sub-dermal angiogenesis.
abstract: The development of a good blood supply is a key step in burn wound healing and appears to be regulated in part by myeloid cells. CX3CR1 positive cells have recently been identified as myeloid cells with a potential role in angiogenesis. The role of functional CX3CR1 system in burn wound healing is not previously investigated. A 2% contact burn was induced in CX3CR1(+/gfp) and CX3CR1(gfp/gfp) mice. These transgenic mice facilitate the tracking of CX3CR1 cells (CX3CR1(+/gfp)) and allow evaluation of the consequence of CX3CR1 functional knockout (CX3CR1(gfp/gfp)) on burn wound healing. The progression of wound healing was monitored before tissue was harvested and analyzed at day 6 and day 12 for migration of CX3CR1 cells into burn wound. Deficiency of a functional CX3CR1 system resulted in decreased recruitment of CX3CR1 positive cells into the burn wound associated with decreased myeloid cell recruitment (p<0.001) and reduced maintenance of new vessels (p<0.001). Burn wound healing was prolonged (p<0.05). Our study is the first to establish a role for CX3CR1 in burn wound healing which is associated with sub-dermal angiogenesis. This chemokine receptor pathway may be attractive for therapeutic manipulation as it could increase sub dermal angiogenesis and thereby improve time to healing.
authors.affiliation: Department of Plastic Surgery, University College Cork, Cork, Ireland. j.clover@ucc.ie
authors.forename: Anthony J P
authors.initials: AJ
authors.lastname: Clover
authors.forename: Arun H S
authors.initials: AH
authors.lastname: Kumar
authors.forename: Noel M
authors.initials: NM
authors.lastname: Caplice
mesh_terms: D000818:Animals; D002056:Burns / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D000073883:CX3C Chemokine Receptor 1; D054428:Chemokine CX3CL1 / Q000378:metabolism; D042783:Endothelial Cells / Q000473:pathology; D007150:Immunohistochemistry; D008264:Macrophages / Q000473:pathology; D051379:Mice; D008822:Mice, Transgenic; D023421:Models, Animal; D022423:Myeloid Cells / Q000473:pathology*; D018919:Neovascularization, Physiologic / Q000502:physiology*; D019707:Receptors, Chemokine / Q000172:deficiency*; D012867:Skin / Q000098:blood supply* / Q000166:cytology; D014945:Wound Healing / Q000502:physiology*
chemical_list: D000073883:CX3C Chemokine Receptor 1; D054428:Chemokine CX3CL1; C471885:Cx3cr1 protein, mouse; D019707:Receptors, Chemokine