Human saliva stimulates skin and oral wound healing in vitro

Abstract

Despite continuous exposure to environmental pathogens, injured mucosa within the oral cavity heals faster and almost scar free compared with skin. Saliva is thought to be one of the main contributing factors. Saliva may possibly also stimulate skin wound healing. If so, it would provide a novel therapy for treating skin wounds, for example, burns. This study aims to investigate the therapeutic wound healing potential of human saliva in vitro. Human saliva from healthy volunteers was filter sterilized before use. Two different in vitro wound models were investigated: (a) open wounds represented by 2D skin and gingiva cultures were used to assess fibroblast and keratinocyte migration and proliferation and (b) blister wounds represented by introducing freeze blisters into organotypic reconstructed human skin and gingiva. Re‐epithelialization and differentiation (keratin K10, K13, K17 expression) under the blister and inflammatory wound healing mediator secretion was assessed. Saliva‐stimulated migration of skin and oral mucosa fibroblasts and keratinocytes, but only fibroblast proliferation. Topical saliva application to the blister wound on reconstructed skin did not stimulate re‐epithelization because the blister wound contained a dense impenetrable dead epidermal layer. Saliva did promote an innate inflammatory response (increased CCL20, IL‐6, and CXCL‐8 secretion) when applied topically to the flanking viable areas of both wounded reconstructed human skin and oral mucosa without altering the skin specific keratin differentiation profile. Our results show that human saliva can stimulate oral and skin wound closure and an inflammatory response. Saliva is therefore a potential novel therapeutic for treating open skin wounds.

Differential influence ofStreptococcus mitison host response to metals in reconstructed human skin and oral mucosa

“…58 Previously we have described intrinsic differences between skin and gingiva with regard to innate immunology, wound healing, and the response to contact sensitizers. 48,[59][60][61] In current study, under unexposed conditions, we show that RHS secretes higher baseline levels of cytokines involved in LC migration (IL-18 and CXCL12) than RHG, which is in line with our previous study, 25,48 and we also show that S. mitis increased the cytokine release of IL-6, CXCL8, CCL5, and CCL20 in RHS but not in RHG. Such relative inertness of RHG to S. mitis is supported by findings of others describing the regulatory role of S. mitis as an oral commensal on immune balance, where it inhibits CD 4+ T cell proliferation, promotes Th17 responses, and induces the secretion of IL-10 in human monocytes.…”

Human serum proteins bind to Sporothrix schenckii conidia with differential effects on phagocytosis

“…Innate immunity is the first line of defence against the microbial infection, where monocytes and macrophages infiltrate the lesion. The binding on the pathogen surface of soluble pattern-recognition proteins sPRPs present in the body fluids guides the pathogen to specific macrophage receptors, which may lead to different cellular responses related to the clearance of the pathogen [12].…”

MicroRNA-31 Can Positively Regulate the Proliferation, Differentiation and Migration of Keratinocytes

“…However, given the existing experimental results, we do not know why the expression level of miR-31 in the oral mucosa is higher than other skin epithelium. Some results show that human saliva can stimulate migration of skin and oral mucosa fibroblasts and keratinocytes to accelerate wound closure and promote an innate inflammatory response (increased CCL20, IL-6, and CXCL-8 secretion) [65]. So, whether there are some special proteins and cytokines in the oral cavity or the digestive environment can induce the high expression of miR-31 to ensure the rapid completion of the wound healing process, this will be a very clinically significant study.…”