Abstract
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 Staphylococcus, Streptococcus, Corynebacterium, Pseudomonas, and several anaerobes. Skin commensal microbes, namely S. epidermidis, can regulate the gamma delta T cells and induce Perforin-2 expression. The increased expression of Perforin-2 by skin cells destroyed S. aureus 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.
Highlights
Short, wound closure is severely impaired in diabetic foot ulcer patients; reduced anIn short, wound closure is severely impaired in diabetic foot ulcer patients; reduced giogenesis is observed due to the hyperglycemic phase, decreased migration of keratinocytes and angiogenesis observed to the hyperglycemic phase,decreasedpoor migration of keratinocytes and fibroblasts, is resulting indue a deficient re-epithelialization; production of the extracellufibroblasts, in a deficient re-epithelialization; poor production lar matrixresulting by fibroblasts contributes to the problem of deficient wound closure.of the extracellular matrix by fibroblasts contributes to the problem of deficient wound closure
Studies have expanded its concept such that, while the diversity of bacteria was independent of chronic wound type, there were more prevalent bacteria such as S. epidermidis identified in patients with diabetic foot ulcers, and Pseudomonas aeruginosa exhibited with a higher relative abundance overall in patients with chronic wounds demonstrating biofilm formation [101]
Based on existing knowledge of wound microbiota in diabetic foot ulcers (DFU) patients, the higher or lower abundance of microbes such as various strains of Staphylococcus spp. with some other anaerobes mentioned above may enable clinicians and scientists to make a thorough diagnosis of individual wounds, which may lead to improved patient prognoses through the selection of optimal treatment strategies that could be used in hospitals
Summary
This is highlighted by a diminution in the diversity of diverse bacterial species, as well as an increase in the abundance of pathogenic bacteria, causing the loss of microbiome physiological functions [15,16] This observed phenomenon is called leaky gut, and sometimes it enables bacterial migration and performs a central role in the growth of gastrointestinal and systemic disorders in humans due to a change in microbial species [13,17]. Probiotics potentially may play a significant role in metabolism, immunomodulation, wound healing, and a variety of inflammatory and infectious disorders and diseases, as per a wealth of evidence. Regardless of their physical differences, the skin and gut have a lot of common physiological features and undertake several functions via cross-talk between both the two compartments [27]. It proposes that certain bacterial species, which are usually non-pathogenic, or at best, are not capable of maintaining a chronic infection when present alone, may co-aggregate symbiotically in a pathogenic biofilm and act synergistically to exacerbate chronic infections [39]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
