title: Dendritic cells modulate burn wound healing by enhancing early proliferation.
abstract: Adequate wound healing is vital for burn patients to reduce the risk of infections and prolonged hospitalization. Dendritic cells (DCs) are antigen presenting cells that release cytokines and are central for the activation of innate and acquired immune responses. Studies have showed their presence in human burn wounds; however, their role in burn wound healing remains to be determined. This study investigated the role of DCs in modulating healing responses within the burn wound. A murine model of full-thickness contact burns was used to study wound healing in the absence of DCs (CD11c promoter-driven diphtheria toxin receptor transgenic mice) and in a DC-rich environment (using fms-like tyrosine kinase-3 ligand, FL- a DC growth factor). Wound closure was significantly delayed in DC-deficient mice and was associated with significant suppression of early cellular proliferation, granulation tissue formation, wound levels of TGFβ1 and formation of CD31+ vessels in healing wounds. In contrast, DC enhancement significantly accelerated early wound closure, associated with increased and accelerated cellular proliferation, granulation tissue formation, and increased TGFβ1 levels and CD31+ vessels in healing wounds. We conclude that DCs play an important role in the acceleration of early wound healing events, likely by secreting factors that trigger the proliferation of cells that mediate wound healing. Therefore, pharmacological enhancement of DCs may provide a therapeutic intervention to facilitate healing of burn wounds.
authors.affiliation: Department of Anesthesiology.
authors.forename: Monika
authors.initials: M
authors.lastname: Vinish
authors.affiliation: Department of Anesthesiology.
authors.forename: Weihua
authors.initials: W
authors.lastname: Cui
authors.affiliation: Management, Policy and Community Health Division, School of Public Health, University of Texas Health Science Center, Houston, Texas.
authors.forename: Eboni
authors.initials: E
authors.lastname: Stafford
authors.affiliation: Department of Biochemistry & Molecular Biology, University of Texas Medical Branch, Galveston, Texas.
authors.forename: Leon
authors.initials: L
authors.lastname: Bae
authors.affiliation: Shriners Hospitals for Children Galveston Burn Unit.|Department of Pathology, University of Texas Medical Branch, Galveston, Texas.
authors.forename: Hal
authors.initials: H
authors.lastname: Hawkins
authors.affiliation: Shriners Hospitals for Children Galveston Burn Unit.|Department of Pathology, University of Texas Medical Branch, Galveston, Texas.
authors.forename: Robert
authors.initials: R
authors.lastname: Cox
authors.affiliation: Department of Anesthesiology.|Shriners Hospitals for Children Galveston Burn Unit.
authors.forename: Tracy
authors.initials: T
authors.lastname: Toliver-Kinsky
mesh_terms: D000276:Adjuvants, Immunologic / Q000494:pharmacology; D000818:Animals; D002056:Burns; D039521:CD11c Antigen; D049109:Cell Proliferation / Q000187:drug effects / Q000502:physiology*; D003713:Dendritic Cells / Q000187:drug effects / Q000502:physiology*; D006097:Granulation Tissue; D066257:Heparin-binding EGF-like Growth Factor / Q000235:genetics; D008297:Male; D008565:Membrane Proteins / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D008822:Mice, Transgenic; D018919:Neovascularization, Physiologic / Q000187:drug effects / Q000502:physiology*; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D011401:Promoter Regions, Genetic; D053773:Transforming Growth Factor beta1 / Q000187:drug effects / Q000378:metabolism; D014945:Wound Healing / Q000187:drug effects / Q000502:physiology*
chemical_list: D000276:Adjuvants, Immunologic; D039521:CD11c Antigen; D066257:Heparin-binding EGF-like Growth Factor; D008565:Membrane Proteins; D019408:Platelet Endothelial Cell Adhesion Molecule-1; C508961:Tgfb1 protein, mouse; D053773:Transforming Growth Factor beta1; C084881:flt3 ligand protein