Control of Innate Immunity, Collaborative Innovation Partnership, Kagawa, Japan.
Macrophi Inc., Kagawa, Japan.
In Vivo. 2024 Sep-Oct;38(5):2172-2178. doi: 10.21873/invivo.13680.
BACKGROUND/AIM: Because the skin is exposed to the external environment, it is important that wound healing processes proceed and terminate rapidly to minimize the risk of infection. A previous case report described the promotion of wound healing by transdermal administration of lipopolysaccharide derived from Pantoea agglomerans (LPSp). However, whether the wound healing-promoting effect of LPSp was due to direct activity on skin cells or indirect effects involving macrophages remained unclear. Therefore, this study investigated the wound healing-promoting effect of LPSp, particularly the promotion of keratinocyte migration.
The migration of HaCaT human keratinocytes over time with and without LPSp was assayed using a cell migration assay kit. Migration was also analyzed using HaCaT cells treated with LPSp and an antibody against Toll-like receptor (TLR) 4, a receptor for LPS.
Addition of LPSp significantly enhanced cell migration compared to no LPSp addition. Migration was inhibited by the addition of anti-TLR4 antibody.
LPSp acts directly on epidermal cells to promote migration and may be one mechanism by which LPSp promotes wound healing.
背景/目的:由于皮肤暴露于外部环境,因此迅速进行并完成伤口愈合过程以最大程度降低感染风险非常重要。之前有病例报告描述了经皮给予成团泛菌(Pantoea agglomerans)来源的脂多糖(LPSp)可促进伤口愈合。然而,LPSp 的促愈合作用是源于对皮肤细胞的直接作用,还是涉及巨噬细胞的间接作用尚不清楚。因此,本研究调查了 LPSp 的促愈合作用,特别是对角质形成细胞迁移的促进作用。
使用细胞迁移检测试剂盒检测有和没有 LPSp 时 HaCaT 人角质形成细胞随时间的迁移。还分析了用 LPSp 和 Toll 样受体(TLR)4 抗体处理的 HaCaT 细胞的迁移,TLR4 是 LPS 的受体。
与不加 LPSp 相比,加入 LPSp 可显著增强细胞迁移。加入抗 TLR4 抗体可抑制迁移。
LPSp 直接作用于表皮细胞以促进迁移,这可能是 LPSp 促进伤口愈合的机制之一。