Patel Bharati Kadamb, Patel Kadamb Haribhai, Huang Ryan Yuki, Lee Chuen Neng, Moochhala Shabbir M
Department of Surgery, National University of Singapore, Singapore 119228, Singapore.
School of Applied Sciences, Temasek Polytechnic, Singapore 529757, Singapore.
Int J Mol Sci. 2022 Feb 21;23(4):2375. doi: 10.3390/ijms23042375.
Diabetic foot ulcers (DFU) are a growing concern worldwide as they pose complications in routine clinical practices such as diagnosis and management. Bacterial interactions on the skin surface are vital to the pathophysiology of DFU and may control delayed wound healing. The microbiota from our skin directly regulates cutaneous health and disease by interacting with the numerous cells involved in the wound healing mechanism. Commensal microbiota, in particular, interact with wound-repairing skin cells to enhance barrier regeneration. The observed microbes in DFU include , , , , and several anaerobes. Skin commensal microbes, namely , can regulate the gamma delta T cells and induce Perforin-2 expression. The increased expression of Perforin-2 by skin cells destroyed within the cells, facilitating wound healing. Possible crosstalk between the human commensal microbiome and different cell types involved in cutaneous wound healing promotes the immune response and helps to maintain the barrier function in humans. Wound healing is a highly well-coordinated, complex mechanism; it can be devastating if interrupted. Skin microbiomes are being studied in relation to the gut-skin axis along with their effects on dermatologic conditions. The gut-skin axis illustrates the connection wherein the gut can impact skin health due to its immunological and metabolic properties. The precise mechanism underlying gut-skin microbial interactions is still unidentified, but the immune and endocrine systems are likely to be involved. Next-generation sequencing and the development of bioinformatics pipelines may considerably improve the understanding of the microbiome-skin axis involved in diabetic wound healing in a much more sophisticated way. We endeavor to shed light on the importance of these pathways in the pathomechanisms of the most prevalent inflammatory conditions including the diabetes wound healing, as well as how probiotics may intervene in the gut-skin axis.
糖尿病足溃疡（DFU）在全球范围内日益受到关注，因为它们在常规临床实践（如诊断和管理）中会引发并发症。皮肤表面的细菌相互作用对DFU的病理生理学至关重要，可能会控制伤口愈合延迟。我们皮肤中的微生物群通过与伤口愈合机制中涉及的众多细胞相互作用，直接调节皮肤健康和疾病。特别是共生微生物群与修复伤口的皮肤细胞相互作用，以增强屏障再生。在DFU中观察到的微生物包括金黄色葡萄球菌、大肠杆菌、铜绿假单胞菌、白色念珠菌和几种厌氧菌。皮肤共生微生物，即表皮葡萄球菌，可以调节γδT细胞并诱导穿孔素-2表达。皮肤细胞中穿孔素-2表达的增加会破坏细胞内的金黄色葡萄球菌，促进伤口愈合。人类共生微生物群与皮肤伤口愈合中涉及的不同细胞类型之间可能存在的串扰会促进免疫反应，并有助于维持人类的屏障功能。伤口愈合是一个高度协调、复杂的机制；如果被打断，可能会造成严重后果。目前正在研究皮肤微生物群与肠-皮肤轴的关系及其对皮肤病的影响。肠-皮肤轴说明了肠道因其免疫和代谢特性而可能影响皮肤健康的联系。肠-皮肤微生物相互作用的精确机制仍未明确，但免疫和内分泌系统可能参与其中。下一代测序和生物信息学管道的发展可能会以一种更为复杂的方式，极大地增进我们对参与糖尿病伤口愈合的微生物群-皮肤轴的理解。我们努力阐明这些途径在包括糖尿病伤口愈合在内的最常见炎症性疾病的发病机制中的重要性，以及益生菌如何干预肠-皮肤轴。
