Advanced glycosylation end products (AGEs) accumulate in diabetic wounds. Interactions between AGEs and their receptor (RAGE) leads to dermatologic problems in diabetes. Macrophage, which plays important roles in wound healing, highly expresses RAGE. Therefore, we investigated whether RAGE-expressing macrophages might be responsible for impaired wound healing on diabetes. We used anti-RAGE antibody applied topically on diabetic wounds. After confirming that wound healing was improved in anti-RAGE antibody group compared with normal mice, our results showed that macrophages appeared insufficient in the early stage and fading away slowly in the later proliferative phase compared with the control group, which was ameliorated in anti-RAGE antibody-applied wounds. Blocking AGE-RAGE signaling also increased neutrophils phagocytized by macrophages and promoted the phenotypic switch of macrophages from proinflammatory to prohealing activities. In vitro, phagocytosis of THP-1 (M0) and lipopolysaccharide- (LPS-) induced (M1) macrophages was impaired by treatment with AGEs, while IL-4- and IL-13-induced (M2) macrophages was not. Finally, AGEs increased the proinflammatory response of M1 macrophages, while inhibiting the polarization and anti-inflammatory functions of M2 macrophages. In conclusion, inhibition of AGE-RAGE signaling improved functional disorders of macrophages in the early inflammatory phase, which promoted the healing of wounds in diabetic mice.
Background: To determine the distribution and antimicrobial susceptibility pattern of pathogenic bacteria in patients with chronic cutaneous wounds on a national scale.Methods: A retrospective study was conducted using the data recorded between January 1, 2018 and January1, 2020 in 195 hospitals across China. After screening the data, 815 patients with chronic wounds were finally analyzed. The data collected included information about the patients' general condition and local cutaneous wound assessments, especially microbial culture and antibiotic susceptibility tests. The analyses were performed using SPSS Version 26.Results: The study included 815 patients (290 [35.6%] females; 63 [50–74] years). The most common causes of chronic cutaneous wounds were diabetes (183, 22.5%), infection (178, 21.8%), and pressure (140, 17.2%). Among these, 521(63.9%) samples tested yielded microbial growth, including 70 (13.4%) polymicrobial infection and 451 (86.6%) monomicrobial infection. The positive rate of microbial culture was highest in wound tissue of ulcers caused by infection (87.6%), followed by pressure (77.1%), diabetes (68.3%), and venous diseases (67.7%). Bates-Jensen wound assessment tool (BWAT) scores >25 and wounds that lasted for more than 3 months had a higher positive rate of microbial culture. BWAT scores >25 and wounds in the rump, perineum, and feet were more likely to exhibit polymicrobial infection. A total of 600 strains were isolated, of which 46.2% (277 strains) were Gram-positive bacteria, 51.3% (308 strains) were Gram-negative bacteria, and 2.5% (15 strains) were fungi. The most common bacterial isolates were Staphylococcus aureus (29.2%), Escherichia coli (11.5%), Pseudomonas aeruginosa (11.0%), Proteus mirabilis (8.0%), and Klebsiella pneumoniae (5.8%). The susceptibility tests showed that 116 cultured bacteria were Multidrug resistant (MDR) strains. The resistance rates of S. aureus were 92.0% (161/175) to penicillin, 58.3% (102/175) to erythromycin, and 50.9% (89/175) to clindamycin. Vancomycin was the most effective antibiotic (0% resistance rate) against all Gram-positive bacteria. Besides, the resistance rates of E. coli were 68.1% (47/69) to ampicillin, 68.1% (47/69) to ciprofloxacin, 60.9% (42/69) to levofloxacin. However, all the isolated Gram-negative bacteria showed low resistance rates to tigecycline (3.9%) and amikacin (3.6%).Conclusions: The distribution of bacteria isolated from chronic cutaneous wounds varies with the BWAT scores, causes, duration, and the location of wounds. Multidrug resistance is a serious health issue, and therefore antibiotics used in chronic wounds must be under strict regulation. Our findings may help clinicians in making informed decisions regarding antibiotic therapy.
Dermatological problems in diabetes might play an important role in the spontaneous ulcers and impaired wound healing that are seen in diabetic patients. Investigation of the cause of diabetic skin disorders is critical for identifying effective treatment. The abdominal full-thickness skin tissues of 33 patients (14 nondiabetic and 19 diabetic) were analyzed. The cell viability and malondialdehyde (MDA) production of fibroblasts were measured after advanced glycosylation end product (AGE)-bovine serum albumin (BSA) exposure. Cutaneous histological observation showed reduced thickness of the diabetic abdominal dermis with morphological characteristics of obscured multilayer epithelium and shortened, thinned, and disorganized collagen fibrils with focal chronic inflammatory cell infiltration when compared with controls of the same age. Accumulation of AGEs in diabetic skin was prominent. Less hydroxyproline, higher myeloperoxidase activity, and increased MDA content were detected in diabetic skin. In vitro, the time- and dose-dependent inhibitory effects of AGE-BSA on fibroblast viability as well as the fact that AGE-BSA could promote MDA production of fibroblasts were shown. It is shown that the accumulation of AGEs in diabetic skin tissue induces an oxidative damage of fibroblasts and acts as an important contributor to the thinner diabetic abdominal dermis. The authors believe that diabetic cutaneous properties at baseline may increase the susceptibility to injury, and diabetic wounds possess atypical origin in the repair process.
Inflammation, initiated by polymorphonuclear neutrophil (PMNs) infiltration, is the first step in wound healing. The aim of this study is to investigate the function of neutrophils in a diabetes-impaired wound healing model and to explore the underlying mechanisms leading to neutrophil dysfunction. Superficial second-degree burns were created in the streptozotocin (STZ)-induced diabetic rat model, and the changes in the levels of advanced glycation end products (AGE), receptor of AGE (RAGE), inflammatory cytokines and oxidative markers, as well as cell apoptosis were determined. The effects of AGE on isolated PMNs were also determined in vitro. We found that deposition of AGE in diabetic rat skin activated the neutrophils before injury. However, the dense inflammatory band failed to form in the diabetic rats after injury. Compared with the controls, enhanced expression of RAGE and accelerated cell apoptosis were observed in the burned skin of diabetic rats. The altered expression pattern of inflammatory cytokines (tumor necrosis factor-alpha and interleukin-8) and oxidative markers (glutathione peroxidase, myeloperoxidase, hydrogen peroxide, and malondialdehyde) between burned skin of diabetic and control rats revealed delayed neutrophil chemotaxis and respiratory burst. Furthermore, the results in vitro showed that exposure to AGE inhibited the viability of PMNs, promoted RAGE production and cell apoptosis, and prevented the migration of PMNs, consistent with the findings in vivo. Besides, AGE-treated neutrophils showed increased secretion of inflammatory cytokines and increased oxidative stress. Combined, our results suggest that an interaction between AGE and its receptors inhibits neutrophil viability and function in the diabetic rat burn model.
Background Burns is a type of injury, caused by unintentional exposure to substances of high temperature, including hot liquid, solid, and objects radiating heat energy, placing a high burden not only on patients’ families but also on national healthcare systems globally. It is difficult for policymakers and clinicians to formulate targeted management strategies for burns because data on current epidemiological patterns worldwide are lacking. Methods Data on burns were obtained from the Global Burden of Disease (GBD) 2019 Study. The incidence, disability-adjusted life years (DALYs), and deaths of burns in 204 countries and regions from 1990 to 2019 were calculated and stratified by sex, age, geographical location, and sociodemographic index (SDI). The estimated annual percentage change (EAPC) of incidence, DALYs, and deaths was calculated to evaluate the temporal trends. All analyses were performed using R software, version 4.1.1, with 2-sided P-values < .05 indicating a statistically significant difference. Results A total of 8,378,122 new cases (95% UI, 6,531,887–10,363,109cases) of burns were identified globally in 2019, which is almost evenly split between men and women, and most of the new cases were concentrated in the 10–19-year age group. Besides, burns account for 111,292 deaths (95% UI, 132,392–88,188) globally in 2019, most of which were concentrated in those aged 1–4 years. The burden of burns measured in DALYs was 7,460,448.65 (95% UI, 5,794,505.89–9,478,717.81) in 2019, of which 67% and 33% could be attributed to YLLs and YLDs, respectively. The EAPC of incidence, DALYs, and deaths were negative, the age-standardized rate (ASR) of incidence, DALYs, and deaths were considered to be decreasing in most of the regions, and the EAPCs were negatively correlated with SDI levels, universal health coverage (UHC), and gross domestic product (GDP). Conclusion Globally, the age-standardized rates of burn incidence, DALYs, and mortality, as well as the number of burn DALYs and death cases will continuously decrease, but the number of new burn cases has an increasing tendency globally. In addition, the EAPCs of burns in incidence, DALYs, and deaths indicated that the burden of burns was considered to be decreasing in most of the regions. And from the relationship of EAPCs with SDI, UHC index, and GDP, indicate that prevention burns not only depend on health spending per capita but also depend on the education level per capita and healthcare system performance, but it does not mean higher health spending corresponds to higher UHC index, which needs high efficiency of translating health spending into individuals health gains.
Traumatic scarring is one of the most common complications after soft tissue injury caused by burns and trauma, which affects tens of millions of people worldwide every year. Traumatic scars diminish the quality of life due to disfigurement, symptoms of pain and itch, and restricted motion. The pathogenesis and pathophysiology of traumatic scar remain elusive. The management for traumatic scars is comprised of surgical and non-surgical interventions such as pressure therapy, silicone, corticosteroid, and radiotherapy, which are chosen by clinicians based on the physical examinations of scars. Recently, great progress in treating traumatic scars has been achieved by the development of novel technologies including laser, intense pulsed light (IPL), radiofrequency, and ultrasound. The aim of this review article was to summarize the advances of these technologies for traumatic scars intervention.
FMRT is an efficacious, safe treatment for non-hypertrophic burn scars in the Asian population. Lasers Surg. Med. 49:563-569, 2017. © 2017 Wiley Periodicals, Inc.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.