Abstract
Lactic acid bacteria (LAB) are known to have beneficial effects on immune responses when they are orally administered as bacterial products. Although the beneficial effects of LAB have been reported for the genera Lactobacillus and Lactococcus, little has been uncovered on the effects of the genus Enterococcus on skin wound-healing. In this study, we aimed to clarify the effect of heat-killed Enterococcus faecalis KH2 (heat-killed KH2) strain on the wound-healing process and to evaluate the therapeutic potential in chronic skin wounds. We analyzed percent wound closure, re-epithelialization, and granulation area, and cytokine and growth factor production. We found that heat-killed KH2 contributed to the acceleration of re-epithelialization and the formation of granulation tissue by inducing tumor necrosis factor-α, interleukin-6, basic fibroblast growth factor, transforming growth factor (TGF)-β1, and vascular endothelial growth factor production. In addition, heat-killed KH2 also improved wound closure, which was accompanied by the increased production of TGF-β1 in diabetic mice. Topical administration of heat-killed KH2 might have therapeutic potential for the treatment of chronic skin wounds in diabetes mellitus. In the present study, we concluded that heat-killed KH2 promoted skin wound-healing through the formation of granulation tissues and the production of inflammatory cytokines and growth factors.
Highlights
To address the possible promotion of wound-healing by heat-killed KH2, we examined the effect of treatment with this bacterium on the wound-healing process in skin
Heat-killed KH2 showed the highest promotion of wound-healing at 500 μg/wound compared to the effect at 5 or 50 μg/wound
The production of vascular endothelial growth factor (VEGF), transforming growth factor (TGF)-β, and basic fibroblast growth factor (bFGF) was reported to be promoted by proinflammatory cytokines, including tumor necrosis factor (TNF)-α and IL-6 [33,34,35]. These results suggest that the enhanced production of VEGF, TGF-β1, and bFGF caused by heat-killed KH2 treatment may be due to the up-regulation of TNF-α and IL-6 production, which may lead to the promotion of re-epithelialization, granulation tissue formation, and angiogenesis
Summary
Wounds are categorized as acute or chronic based on the time it takes them to heal. Acute wounds generally heal within 2 weeks whereas chronic wounds can take several months or longer. Acute wound-healing in the skin moves through inflammation, proliferation, and remodeling phases [1]. Keratinocytes, fibroblasts, and leukocytes produce inflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, which are important for leukocyte recruitment and protection against infection [2,3]. Numerous growth factors, such as Biomedicines 2021, 9, 1520.
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