PDF(Pubmed)
Abstract：
Chronic wounds are a common and costly complication of diabetes, where multifactorial defects contribute to dysregulated skin repair, inflammation, tissue damage, and infection. We previously showed that aspects of the diabetic foot ulcer microbiota were correlated with poor healing outcomes, but many microbial species recovered remain uninvestigated with respect to wound healing. Here, we focused on Alcaligenes faecalis, a Gram-negative bacterium that is frequently recovered from chronic wounds but rarely causes infection. Treatment of diabetic wounds with A. faecalis accelerated healing during early stages. We investigated the underlying mechanisms and found that A. faecalis treatment promotes reepithelialization of diabetic keratinocytes, a process that is necessary for healing but deficient in chronic wounds. Overexpression of matrix metalloproteinases in diabetes contributes to failed epithelialization, and we found that A. faecalis treatment balances this overexpression to allow proper healing. This work uncovers a mechanism of bacterial-driven wound repair and provides a foundation for the development of microbiota-based wound interventions.
摘要：
慢性伤口是糖尿病常见且昂贵的并发症，多因素缺陷导致皮肤修复失调，炎症,组织损伤,和感染。我们以前表明，糖尿病足溃疡微生物群的各个方面与不良的愈合结果相关，但是在伤口愈合方面，许多回收的微生物物种仍未被研究。这里,我们专注于粪产碱菌，一种革兰氏阴性细菌，通常从慢性伤口中恢复，但很少引起感染。在早期阶段用粪肠杆菌治疗糖尿病伤口加速愈合。我们研究了潜在的机制，发现粪肠杆菌治疗促进糖尿病角质形成细胞的再上皮化，一个过程，是必要的愈合，但缺乏慢性伤口。糖尿病中基质金属蛋白酶的过度表达导致上皮形成失败，我们发现粪肠杆菌治疗平衡了这种过度表达以允许适当的愈合。这项工作揭示了细菌驱动的伤口修复机制，并为开发基于微生物群的伤口干预措施奠定了基础。
