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The impact of gut microbiota changes on the intestinal mucus barrier in burned mice: a study using 16S rRNA and metagenomic sequencing. 肠道微生物群变化对烧伤小鼠肠道粘液屏障的影响:一项使用 16S rRNA 和元基因组测序的研究。
IF 5.3 1区 医学 Q1 Medicine Pub Date : 2023-12-19 eCollection Date: 2023-01-01 DOI: 10.1093/burnst/tkad056
Xule Zha, Sen Su, Dan Wu, Panyang Zhang, Yan Wei, Shijun Fan, Qianying Huang, Xi Peng

Background: The gut microbiota is a complex ecosystem that plays a critical role in human health and disease. However, the relationship between gut microbiota and intestinal damage caused by burns is not well understood. The intestinal mucus layer is crucial for maintaining intestinal homeostasis and providing a physiological barrier against bacterial invasion. This study aims to investigate the impact of gut microbiota on the synthesis and degradation of intestinal mucus after burns and explore potential therapeutic targets for burn injury.

Methods: A modified histopathological grading system was employed to investigate the effects of burn injury on colon tissue and the intestinal mucus barrier in mice. Subsequently, 16S ribosomal RNA sequencing was used to analyze alterations in the gut microbiota at days 1-10 post-burn. Based on this, metagenomic sequencing was conducted on samples collected at days 1, 5 and 10 to investigate changes in mucus-related microbiota and explore potential underlying mechanisms.

Results: Our findings showed that the mucus barrier was disrupted and that bacterial translocation occurred on day 3 following burn injury in mice. Moreover, the gut microbiota in mice was significantly disrupted from days 1 to 3 following burn injury, but gradually recovered to normal as the disease progressed. Specifically, there was a marked increase in the abundance of symbiotic and pathogenic bacteria associated with mucin degradation on day 1 after burns, but the abundance returned to normal on day 5. Conversely, the abundance of probiotic bacteria associated with mucin synthesis changed in the opposite direction. Further analysis revealed that after a burn injury, bacteria capable of degrading mucus may utilize glycoside hydrolases, flagella and internalins to break down the mucus layer, while bacteria that synthesize mucus may help restore the mucus layer by promoting the production of short-chain fatty acids.

Conclusions: Burn injury leads to disruption of colonic mucus barrier and dysbiosis of gut microbiota. Some commensal and pathogenic bacteria may participate in mucin degradation via glycoside hydrolases, flagella, internalins, etc. Probiotics may provide short-chain fatty acids (particularly butyrate) as an energy source for stressed intestinal epithelial cells, promote mucin synthesis and accelerate repair of mucus layer.

背景:肠道微生物群是一个复杂的生态系统,在人类健康和疾病中发挥着至关重要的作用。然而,人们对肠道微生物群与烧伤造成的肠道损伤之间的关系还不甚了解。肠道粘液层对维持肠道平衡和提供防止细菌入侵的生理屏障至关重要。本研究旨在探讨肠道微生物群对烧伤后肠粘液合成和降解的影响,并探索烧伤的潜在治疗靶点:方法:采用改良的组织病理学分级系统研究烧伤对小鼠结肠组织和肠粘液屏障的影响。随后,采用 16S 核糖体 RNA 测序分析烧伤后第 1-10 天肠道微生物群的变化。在此基础上,对第 1、5 和 10 天采集的样本进行了元基因组测序,以研究粘液相关微生物群的变化并探索潜在的内在机制:结果:我们的研究结果表明,小鼠烧伤后第 3 天,粘液屏障遭到破坏,细菌发生迁移。此外,小鼠的肠道微生物群在烧伤后第 1 到 3 天受到严重破坏,但随着病情的发展逐渐恢复正常。具体来说,烧伤后第 1 天,与粘蛋白降解相关的共生菌和致病菌的数量明显增加,但第 5 天又恢复正常。相反,与粘蛋白合成相关的益生菌的数量却发生了相反的变化。进一步分析表明,烧伤后,能够降解粘液的细菌可能会利用糖苷水解酶、鞭毛和内毒素来分解粘液层,而合成粘液的细菌可能会通过促进短链脂肪酸的产生来帮助恢复粘液层:结论:烧伤导致结肠粘液屏障破坏和肠道微生物群失调。一些共生菌和致病菌可能通过糖苷水解酶、鞭毛、内蛋白等参与粘蛋白降解。益生菌可提供短链脂肪酸(尤其是丁酸盐),作为受压肠道上皮细胞的能量来源,促进粘蛋白的合成,加快粘液层的修复。
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引用次数: 0
The clinical differentiation of blood culture-positive and -negative sepsis in burn patients: a retrospective cohort study 烧伤患者血培养阳性和阴性败血症的临床鉴别:一项回顾性队列研究
IF 5.3 1区 医学 Q1 Medicine Pub Date : 2023-12-19 DOI: 10.1093/burnst/tkad031
Jaechul Yoon, Dohern Kym, Jun Hur, Jongsoo Park, Myongjin Kim, Yong Suk Cho, Wook Chun, Dogeon Yoon
Background Sepsis is a potentially life-threatening condition that occurs when the body’s response to infection leads to widespread inflammation and tissue damage. Negative cultures can make it difficult for clinicians to make a diagnosis and may raise questions about the validity of the definition of sepsis. In addition, the clinical distinctions between burn patients with blood culture-positive and -negative sepsis are also poorly understood. Therefore, this study aimed to examine the clinical differences between blood culture-positive and -negative sepsis in burn patients in order to improve the understanding of the pathophysiology and epidemiology of sepsis in this population. Methods This study had a retrospective design, and the participants were adults aged ≥18 years. Patients diagnosed with sepsis were divided into two groups based on their blood culture results within 1 week of sepsis diagnosis. Results We enrolled 1643 patients admitted to our institution’s burn intensive care unit between January 2010 and December 2021. pH, platelet count, bicarbonate and haematocrit were significant in both the positive and negative groups. However, lymphocyte, red cell distribution width and blood urea nitrogen were significant only in the positive group, whereas lactate dehydrogenase was significant only in the negative group. Acinetobacter baumannii, Pseudomonas aeruginosa, and Klebsiella pneumonia are common gram-negative bacterial species, and Staphylococcus aureus and Staphylococcus epidermidis are common gram-positive bacterial species seen in burn patients with positive blood cultures. Carbapenem resistance was found to be associated with an unfavourable prognosis in gram-negative bacteria, with the exception of P. aeruginosa. Conclusions pH, platelet count, bicarbonate and haematocrit were routine biomarkers that demonstrated statistical significance in both groups. Lactate dehydrogenase was significant in the blood-negative group, while red cell distribution width, blood urea nitrogen and lymphocyte count were significant in the positive group. Furthermore, the most common causes of sepsis are gram-negative bacteria, including A. baumannii, K. pneumoniae and P. aeruginosa. Additionally, resistance to carbapenems is associated with unfavourable outcomes.
背景败血症是一种可能危及生命的疾病,当机体对感染的反应导致广泛的炎症和组织损伤时就会发生败血症。培养阴性会使临床医生难以做出诊断,并可能对败血症定义的有效性产生疑问。此外,人们对烧伤患者血培养阳性和阴性败血症之间的临床区别也知之甚少。因此,本研究旨在探讨烧伤患者血培养阳性和阴性败血症之间的临床差异,以加深对该人群败血症病理生理学和流行病学的了解。方法 本研究采用回顾性设计,参与者为年龄≥18 岁的成年人。根据败血症确诊后 1 周内的血液培养结果,将确诊为败血症的患者分为两组。pH 值、血小板计数、碳酸氢盐和血细胞比容在阳性组和阴性组均有显著性差异。然而,只有阳性组的淋巴细胞、红细胞分布宽度和血尿素氮有显著性差异,而只有阴性组的乳酸脱氢酶有显著性差异。鲍曼不动杆菌、铜绿假单胞菌和肺炎克雷伯菌是常见的革兰氏阴性菌种,金黄色葡萄球菌和表皮葡萄球菌是烧伤患者血液培养阳性中常见的革兰氏阳性菌种。除铜绿假单胞菌外,碳青霉烯耐药性与革兰氏阴性菌的不良预后有关。结论 pH 值、血小板计数、碳酸氢盐和血细胞比容是常规生物标志物,在两组中均有统计学意义。乳酸脱氢酶在血阴性组有显著意义,而红细胞分布宽度、血尿素氮和淋巴细胞计数在血阳性组有显著意义。此外,败血症最常见的病因是革兰氏阴性菌,包括鲍曼不动杆菌、肺炎双球菌和铜绿假单胞菌。此外,对碳青霉烯类抗生素的耐药性与不利的预后有关。
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引用次数: 0
Plasma lipidomics reveal systemic changes persistent throughout early life following a childhood burn injury 血浆脂质组学揭示了儿童烧伤后整个生命早期持续存在的系统性变化
IF 5.3 1区 医学 Q1 Medicine Pub Date : 2023-12-07 DOI: 10.1093/burnst/tkad044
Eva Kierath, Monique Ryan, Elaine Holmes, Jeremy K Nicholson, Mark W Fear, Fiona M Wood, Luke Whiley, Nicola Gray
Background Non-severe paediatric burns can result in poor long-term health outcomes. This occurs even in cases with good acute burn-related outcomes, including minimal scarring. The mechanisms that underpin the transition from non-severe burn to sustained negative long-term health impacts are currently unknown. However, sustained metabolic and immune changes have been observed in paediatric burn studies, suggesting these changes may be important. The plasma lipidome consists of a rich pool of bioactive metabolites that play critical roles in systemic processes including molecular signalling and inflammation. We hypothesised that changes in the plasma lipidome may reflect underlying changes in health status and be linked to long-term health after burn trauma. Methods This study analysed the lipidome in children who had previously experienced a non-severe burn, compared to non-injured controls. Thirty-three participants were recruited between the ages of 5 and 8 years who had experienced a non-severe burn between the ages of 1 and 3 years. Plasma samples were also collected from a non-injured, healthy, age and gender matched control group (n = 21). Plasma lipids were measured using reversed-phase liquid chromatographymass spectrometery (LC-MS). Results In total 838 reproducible lipid species from 19 sub-classes passed quality control procedures and progressed to statistical analysis. Analysis of individual lipid metabolites showed significantly higher concentrations of lysophosphatidylethanolamines and phosphatidylethanolamines, and significantly lower concentrations in myristic, palmitic and palmitoleic acids in the plasma of those who had experienced burn injury compared to controls. Conclusion Long-term changes in the lipid profile may give insight into the mechanisms underlying poor long-term health subsequent to non-severe burn injury. Further work to investigate the relationship between long-term pathology and lipidomic changes may lead to a better understanding of the causes of secondary morbidity post-burn and to clinical intervention to reduce the long-term health burden of burn trauma.
背景非重度小儿烧伤可能导致不良的长期健康后果。即使在急性烧伤相关结果良好(包括瘢痕最小)的病例中也会出现这种情况。目前尚不清楚从非严重烧伤转变为持续的长期负面健康影响的机制。不过,在儿科烧伤研究中观察到了持续的新陈代谢和免疫变化,这表明这些变化可能很重要。血浆脂质体由丰富的生物活性代谢物组成,在包括分子信号传导和炎症在内的全身过程中发挥着关键作用。我们假设血浆脂质体的变化可能反映了健康状况的潜在变化,并与烧伤后的长期健康状况有关。方法 本研究分析了曾经历过非严重烧伤的儿童与未受伤的对照组儿童的血脂组。研究人员招募了 33 名年龄在 5 到 8 岁之间、在 1 到 3 岁之间经历过非严重烧伤的儿童。此外,还从未受损伤、健康、年龄和性别匹配的对照组(21 人)中采集了血浆样本。血浆脂质采用反相液相色谱-质谱法(LC-MS)进行测量。结果 共有 19 个亚类的 838 种可重复脂质通过了质量控制程序并进入统计分析。对单个脂质代谢物的分析表明,与对照组相比,烧伤患者血浆中溶血磷脂酰乙醇胺和磷脂酰乙醇胺的浓度明显较高,肉豆蔻酸、棕榈酸和棕榈油酸的浓度明显较低。结论 脂质谱的长期变化可能有助于了解非严重烧伤后长期健康状况不佳的机制。进一步研究长期病理变化与脂质组变化之间的关系,可能有助于更好地了解烧伤后继发性发病的原因,并有助于采取临床干预措施,减轻烧伤创伤对健康造成的长期负担。
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引用次数: 0
The impact of COVID-19 on clinical outcomes of burn patients COVID-19 对烧伤患者临床疗效的影响
IF 5.3 1区 医学 Q1 Medicine Pub Date : 2023-12-07 DOI: 10.1093/burnst/tkad042
Elliot T Walters, Alen Palackic, Camila Franco-Mesa, Nikhil R Shah, Michael J Erickson, Steven E Wolf
Background Multiple studies have shown the SARS-CoV-2 virus (COVID-19) to be associated with deleterious outcomes in a wide range of patients. The impact of COVID-19 has not been well investigated among burned patients. We suspect that patients will have worsened respiratory and thrombotic complications, ultimately leading to increased mortality. The objective of this study is to determine the impact a concurrent infection of COVID-19 has on clinical outcomes after a burn injury. Methods This is a retrospective, propensity matched, cohort study. We examined a de-identified database of electronic medical records of over 75 million patients across 75 health care associations in the United States for patients treated for thermal burns from 1 January 2020, to 31 July 2021, and those who also were diagnosed with COVID-19 infection within one day before or after injury based on International Classification of Disease, tenth revision (ICD-10) codes. Study participants included adults who were treated for a burn injury during the study period. Results We included 736 patients with burn injury and concomitant COVID-19 infection matched to 736 patients with burn injury and no concurrent COVID-19 infection (total 1472 patients, mean age 36.3 ± 24.3). We found no significant increase in mortality observed for patients with concurrent COVID-19 (OR 1.203, 95% CI 0.517–2.803; p = 0.6675). We did observe significant increase in infections (OR 3.537, 95% CI 2.798–4.471; p = 0.0001), thrombotic complications (OR 2.342, 95% CI 1.351–4.058; p = 0.0018), as was the incidence of hypertrophic scarring (OR 3.368, 95% CI 2.326–4.877; p = 0.0001). Conclusions We observed that concurrent COVID-19 infection was associated with an increase in infections, thrombosis and hypertrophic scarring but no increase in mortality in our cohort of burn patients.
背景多项研究表明,SARS-CoV-2 病毒(COVID-19)与许多患者的不良预后有关。COVID-19 对烧伤患者的影响尚未得到很好的研究。我们怀疑患者的呼吸系统和血栓并发症会恶化,最终导致死亡率上升。本研究的目的是确定 COVID-19 并发感染对烧伤后临床结果的影响。方法 这是一项倾向匹配的回顾性队列研究。我们对美国 75 家医疗保健协会超过 7500 万名患者的电子病历进行了去标识化数据库检查,以了解 2020 年 1 月 1 日至 2021 年 7 月 31 日期间接受热烧伤治疗的患者,以及根据国际疾病分类第十次修订版(ICD-10)代码在受伤前后一天内被诊断出感染 COVID-19 的患者。研究对象包括在研究期间接受过烧伤治疗的成年人。结果 我们纳入了 736 名烧伤并发 COVID-19 感染的患者和 736 名烧伤但未并发 COVID-19 感染的患者(共 1472 名患者,平均年龄为 36.3 ± 24.3)。我们发现并发 COVID-19 感染的患者死亡率没有明显增加(OR 1.203,95% CI 0.517-2.803;P = 0.6675)。但我们观察到感染(OR 3.537,95% CI 2.798-4.471;p = 0.0001)、血栓并发症(OR 2.342,95% CI 1.351-4.058;p = 0.0018)和增生性瘢痕的发生率(OR 3.368,95% CI 2.326-4.877;p = 0.0001)明显增加。结论 我们观察到,在我们的烧伤患者队列中,并发 COVID-19 感染与感染、血栓形成和增生性瘢痕的增加有关,但死亡率没有增加。
{"title":"The impact of COVID-19 on clinical outcomes of burn patients","authors":"Elliot T Walters, Alen Palackic, Camila Franco-Mesa, Nikhil R Shah, Michael J Erickson, Steven E Wolf","doi":"10.1093/burnst/tkad042","DOIUrl":"https://doi.org/10.1093/burnst/tkad042","url":null,"abstract":"Background Multiple studies have shown the SARS-CoV-2 virus (COVID-19) to be associated with deleterious outcomes in a wide range of patients. The impact of COVID-19 has not been well investigated among burned patients. We suspect that patients will have worsened respiratory and thrombotic complications, ultimately leading to increased mortality. The objective of this study is to determine the impact a concurrent infection of COVID-19 has on clinical outcomes after a burn injury. Methods This is a retrospective, propensity matched, cohort study. We examined a de-identified database of electronic medical records of over 75 million patients across 75 health care associations in the United States for patients treated for thermal burns from 1 January 2020, to 31 July 2021, and those who also were diagnosed with COVID-19 infection within one day before or after injury based on International Classification of Disease, tenth revision (ICD-10) codes. Study participants included adults who were treated for a burn injury during the study period. Results We included 736 patients with burn injury and concomitant COVID-19 infection matched to 736 patients with burn injury and no concurrent COVID-19 infection (total 1472 patients, mean age 36.3 ± 24.3). We found no significant increase in mortality observed for patients with concurrent COVID-19 (OR 1.203, 95% CI 0.517–2.803; p = 0.6675). We did observe significant increase in infections (OR 3.537, 95% CI 2.798–4.471; p = 0.0001), thrombotic complications (OR 2.342, 95% CI 1.351–4.058; p = 0.0018), as was the incidence of hypertrophic scarring (OR 3.368, 95% CI 2.326–4.877; p = 0.0001). Conclusions We observed that concurrent COVID-19 infection was associated with an increase in infections, thrombosis and hypertrophic scarring but no increase in mortality in our cohort of burn patients.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2023-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138550686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Is the surgical community prepared to face patients with SARS-CoV-2-induced cell death and organ injury in the post-pandemic era? 面对由 SARS-CoV-2 引起的细胞死亡和器官损伤的患者,外科界是否做好了后大流行时代的准备?
IF 5.3 1区 医学 Q1 Medicine Pub Date : 2023-11-22 eCollection Date: 2023-01-01 DOI: 10.1093/burnst/tkad049
Sanketh Rampes, Sufia Ruhomaun, Qiang Shu, Daqing Ma
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引用次数: 0
Regulated necrosis pathways: a potential target for ischemic stroke. 受调节的坏死途径:缺血性卒中的潜在靶点。
IF 5.3 1区 医学 Q1 Medicine Pub Date : 2023-11-18 eCollection Date: 2023-01-01 DOI: 10.1093/burnst/tkad016
Kaidi Ren, Jinyan Pei, Yuanyuan Guo, Yuxue Jiao, Han Xing, Yi Xie, Yang Yang, Qi Feng, Jing Yang

Globally, ischemic stroke causes millions of deaths per year. The outcomes of ischemic stroke are largely determined by the amount of ischemia-related and reperfusion-related neuronal death in the infarct region. In the infarct region, cell injuries follow either the regulated pathway involving precise signaling cascades, such as apoptosis and autophagy, or the nonregulated pathway, which is uncontrolled by any molecularly defined effector mechanisms such as necrosis. However, numerous studies have recently found that a certain type of necrosis can be regulated and potentially modified by drugs and is nonapoptotic; this type of necrosis is referred to as regulated necrosis. Depending on the signaling pathway, various elements of regulated necrosis contribute to the development of ischemic stroke, such as necroptosis, pyroptosis, ferroptosis, pathanatos, mitochondrial permeability transition pore-mediated necrosis and oncosis. In this review, we aim to summarize the underlying molecular mechanisms of regulated necrosis in ischemic stroke and explore the crosstalk and interplay among the diverse types of regulated necrosis. We believe that targeting these regulated necrosis pathways both pharmacologically and genetically in ischemia-induced neuronal death and protection could be an efficient strategy to increase neuronal survival and regeneration in ischemic stroke.

在全球范围内,缺血性中风每年造成数百万人死亡。缺血性脑卒中的预后在很大程度上取决于梗死区缺血相关和再灌注相关神经元死亡的数量。在梗死区,细胞损伤要么遵循包括精确信号级联的调控途径,如凋亡和自噬,要么遵循不受任何分子效应机制(如坏死)控制的非调控途径。然而,最近大量研究发现,某种类型的坏死可以被药物调节和潜在地修饰,并且是非凋亡性的;这种类型的坏死被称为调节性坏死。根据信号通路的不同,各种受调控的坏死因子参与缺血性卒中的发展,如坏死性坏死、焦性坏死、铁性坏死、病理坏死、线粒体通透性转移、孔介导的坏死和肿瘤。在本文中,我们旨在总结缺血性脑卒中中调控性坏死的潜在分子机制,并探讨不同类型的调控性坏死之间的相互作用。我们认为,在缺血诱导的神经元死亡和保护中,从药理学和遗传学上靶向这些受调节的坏死途径可能是增加缺血性卒中中神经元存活和再生的有效策略。
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引用次数: 0
Extracellular vesicles modulate key signalling pathways in refractory wound healing 细胞外囊泡调节难治性伤口愈合的关键信号通路
IF 5.3 1区 医学 Q1 Medicine Pub Date : 2023-11-17 DOI: 10.1093/burnst/tkad039
Bowen Yang, Yumeng Lin, Yibo Huang, Nanxi Zhu, Ying-Qiang Shen
Chronic wounds are wounds that cannot heal properly due to various factors, such as underlying diseases, infection or reinjury, and improper healing of skin wounds and ulcers can cause a serious economic burden. Numerous studies have shown that extracellular vesicles (EVs) derived from stem/progenitor cells promote wound healing, reduce scar formation and have significant advantages over traditional treatment methods. EVs are membranous particles that carry various bioactive molecules from their cellular origins, such as cytokines, nucleic acids, enzymes, lipids and proteins. EVs can mediate cell-to-cell communication and modulate various physiological processes, such as cell differentiation, angiogenesis, immune response and tissue remodelling. In this review, we summarize the recent advances in EV-based wound healing, focusing on the signalling pathways that are regulated by EVs and their cargos. We discuss how EVs derived from different types of stem/progenitor cells can promote wound healing and reduce scar formation by modulating the Wnt/β-catenin, phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin, vascular endothelial growth factor, transforming growth factor β and JAK–STAT pathways. Moreover, we also highlight the challenges and opportunities for engineering or modifying EVs to enhance their efficacy and specificity for wound healing.
慢性伤口是指由于潜在疾病、感染或再损伤等多种因素导致无法正常愈合的伤口,皮肤伤口和溃疡愈合不当会造成严重的经济负担。大量研究表明,来自干细胞/祖细胞的细胞外囊泡(EVs)促进伤口愈合,减少疤痕形成,与传统治疗方法相比具有显著优势。电动汽车是一种膜状颗粒,携带来自细胞起源的各种生物活性分子,如细胞因子、核酸、酶、脂质和蛋白质。电动汽车可以介导细胞间的通讯,调节各种生理过程,如细胞分化、血管生成、免疫反应和组织重塑。在这篇综述中,我们总结了基于电动汽车的伤口愈合的最新进展,重点是由电动汽车及其货物调节的信号通路。我们讨论了来自不同类型的干细胞/祖细胞的ev如何通过调节Wnt/β-连环蛋白、磷酸肌肽3-激酶/蛋白激酶B/雷帕霉素的哺乳动物靶点、血管内皮生长因子、转化生长因子β和JAK-STAT途径促进伤口愈合和减少疤痕形成。此外,我们还强调了工程或改造电动汽车以提高其伤口愈合的功效和特异性的挑战和机遇。
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引用次数: 0
Peptide RL-QN15 promotes wound healing of diabetic foot ulcers through p38 mitogen-activated protein kinase and smad3/miR-4482-3p/vascular endothelial growth factor B axis 肽RL-QN15通过p38丝裂原活化蛋白激酶和smad3/miR-4482-3p/血管内皮生长因子B轴促进糖尿病足溃疡创面愈合
IF 5.3 1区 医学 Q1 Medicine Pub Date : 2023-11-17 DOI: 10.1093/burnst/tkad035
Dandan Sun, Kun Guo, Naixin Liu, Yilin Li, Yuansheng Li, Yan Hu, Shanshan Li, Zhe Fu, Yinglei Wang, Yutong Wu, Yingxuan Zhang, Jiayi Li, Chao Li, Zhuo Wang, Zijian Kang, Jun Sun, Ying Wang, Xinwang Yang
Background Wound management of diabetic foot ulcers (DFUs) is a complex and challenging task, and existing strategies fail to meet clinical needs. Therefore, it is important to develop novel drug candidates and discover new therapeutic targets. However, reports on peptides as molecular probes for resolving issues related to DFUs remain rare. This study utilized peptide RL-QN15 as an exogenous molecular probe to investigate the underlying mechanism of endogenous non-coding RNA in DFU wound healing. The aim was to generate novel insights for the clinical management of DFUs and identify potential drug targets. Methods We investigated the wound-healing efficiency of peptide RL-QN15 under diabetic conditions using in vitro and in vivo experimental models. RNA sequencing, in vitro transfection, quantitative real-time polymerase chain reaction, western blotting, dual luciferase reporter gene detection, in vitro cell scratches, and cell proliferation and migration assays were performed to explore the potential mechanism underlying the promoting effects of RL-QN15 on DFU repair. Results Peptide RL-QN15 enhanced the migration and proliferation of human immortalized keratinocytes (HaCaT cells) in a high-glucose environment and accelerated wound healing in a DFU rat model. Based on results from RNA sequencing, we defined a new microRNA (miR-4482-3p) related to the promotion of wound healing. The bioactivity of miR-4482-3p was verified by inhibiting and overexpressing miR-4482-3p. Inhibition of miR-4482-3p enhanced the migration and proliferation ability of HaCaT cells as well as the expression of vascular endothelial growth factor B (VEGFB). RL-QN15 also promoted the migration and proliferation ability of HaCaT cells, and VEGFB expression was mediated via inhibition of miR-4482-3p expression by the p38 mitogen-activated protein kinase (p38MAPK) and smad3 signaling pathways. Conclusions RL-QN15 is an effective molecule for the treatment of DFUs, with the underlying mechanism related to the inhibition of miR-4482-3p expression via the p38MAPK and smad3 signaling pathways, ultimately promoting re-epithelialization, angiogenesis and wound healing. This study provides a theoretical basis for the clinical application of RL-QN15 as a molecular probe in promoting DFU wound healing.
背景:糖尿病足溃疡(DFUs)的伤口管理是一项复杂而具有挑战性的任务,现有的策略不能满足临床需要。因此,开发新的候选药物和发现新的治疗靶点非常重要。然而,关于多肽作为分子探针解决dfu相关问题的报道仍然很少。本研究利用肽RL-QN15作为外源性分子探针,探讨内源性非编码RNA在DFU创面愈合中的潜在机制。目的是为DFUs的临床管理产生新的见解,并确定潜在的药物靶点。方法采用体外和体内实验模型,研究肽RL-QN15对糖尿病患者创面愈合的影响。通过RNA测序、体外转染、实时定量聚合酶链反应、western blotting、双荧光素酶报告基因检测、体外细胞划痕、细胞增殖和迁移等实验,探讨RL-QN15促进DFU修复的可能机制。结果肽RL-QN15增强了人永生化角质形成细胞(HaCaT细胞)在高糖环境下的迁移和增殖,加速了DFU大鼠模型的伤口愈合。根据RNA测序结果,我们定义了一种新的与促进伤口愈合相关的microRNA (miR-4482-3p)。通过抑制和过表达miR-4482-3p来验证miR-4482-3p的生物活性。抑制miR-4482-3p可增强HaCaT细胞的迁移和增殖能力以及血管内皮生长因子B (VEGFB)的表达。RL-QN15还能促进HaCaT细胞的迁移和增殖能力,通过p38丝裂原活化蛋白激酶(p38MAPK)和smad3信号通路抑制miR-4482-3p表达介导VEGFB的表达。结论RL-QN15是治疗DFUs的有效分子,其机制可能与通过p38MAPK和smad3信号通路抑制miR-4482-3p的表达有关,最终促进再上皮化、血管生成和伤口愈合。本研究为RL-QN15作为分子探针促进DFU创面愈合的临床应用提供了理论依据。
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引用次数: 0
Chinese expert consensus on the Management of Pediatric Deep Partial-Thickness Burn Wounds (2023 edition). 中国儿科深部偏厚烧伤创面管理专家共识(2023年版)。
IF 5.3 1区 医学 Q1 Medicine Pub Date : 2023-10-31 eCollection Date: 2023-01-01 DOI: 10.1093/burnst/tkad053
Yan Liu

Burns are a main cause of accidental injuries among children in China. Because of the unique wound repair capacity and demand for growth in pediatric patients, the management of pediatric deep partial-thickness burn wounds involves a broader range of treatment options and controversy. We assembled experts from relevant fields in China to reach a consensus on the key points of thermal-induced pediatric deep partial-thickness burn-wound management, including definition and diagnosis, surgical treatments, nonsurgical treatment, choice of wound dressings, growth factor applications, infectious wound treatment, scar prevention and treatment. The committee members hope that the Expert Consensus will provide help and guiding recommendations for the treatment of pediatric deep partial-thickness burn wounds.

烧伤是中国儿童意外伤害的主要原因。由于儿科患者独特的伤口修复能力和成长需求,儿科深部部分厚度烧伤伤口的管理涉及更广泛的治疗选择和争议。我们汇集了国内相关领域的专家,就热致儿童深部偏厚烧伤创面管理的关键点达成共识,包括定义和诊断、手术治疗、非手术治疗、创面敷料的选择、生长因子的应用、感染性创面治疗、瘢痕预防和治疗。委员会成员希望《专家共识》将为儿科深部部分厚度烧伤的治疗提供帮助和指导性建议。
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引用次数: 0
S100 calcium-binding protein A9 promotes skin regeneration through toll-like receptor 4 during tissue expansion. S100钙结合蛋白A9在组织扩张过程中通过toll样受体4促进皮肤再生。
IF 5.3 1区 医学 Q1 Medicine Pub Date : 2023-10-31 eCollection Date: 2023-01-01 DOI: 10.1093/burnst/tkad030
Yu Zhang, Yajuan Song, Jing Du, Wei Liu, Chen Dong, Zhaosong Huang, Zhe Zhang, Liu Yang, Tong Wang, Shaoheng Xiong, Liwei Dong, Yaotao Guo, Juanli Dang, Qiang He, Zhou Yu, Xianjie Ma

Background: In plastic surgery, tissue expansion is widely used for repairing skin defects. However, low expansion efficiency and skin rupture caused by thin, expanded skin remain significant challenges in promoting skin regeneration during expansion. S100 calcium-binding protein A9 (S100A9) is essential in promoting wound healing; however, its effects on skin regeneration during tissue expansion remain unclear. The aim of the present study was to explore the role of S100A9 in skin regeneration, particularly collagen production to investigate its importance in skin regeneration during tissue expansion.

Methods: The expression and distribution of S100A9 and its receptors-toll-like receptor 4 (TLR-4) and receptor for advanced glycation end products were studied in expanded skin. These characteristics were investigated in skin samples of rats and patients. Moreover, the expression of S100A9 was investigated in stretched keratinocytes in vitro. The effects of S100A9 on the proliferation and migration of skin fibroblasts were also observed. TAK-242 was used to inhibit the binding of S100A9 to TLR-4; the levels of collagen I (COL I), transforming growth factor beta (TGF-β), TLR-4 and phospho-extracellular signal-related kinase 1/2 (p-ERK1/2) in fibroblasts were determined. Furthermore, fibroblasts were co-cultured with stretched S100A9-knockout keratinocytes by siRNA transfection and the levels of COL I, TGF-β, TLR-4 and p-ERK1/2 in fibroblasts were investigated. Additionally, the area of expanded skin, thickness of the dermis, and synthesis of COL I, TGF-β, TLR-4 and p-ERK1/2 were analysed to determine the effects of S100A9 on expanded skin.

Results: Increased expression of S100A9 and TLR-4 was associated with decreased extracellular matrix (ECM) in the expanded dermis. Furthermore, S100A9 facilitated the proliferation and migration of human skin fibroblasts as well as the expression of COL I and TGF-β in fibroblasts via the TLR-4/ERK1/2 pathway. We found that mechanical stretch-induced S100A9 expression and secretion of keratinocytes stimulated COL I, TGF-β, TLR-4 and p-ERK1/2 expression in skin fibroblasts. Recombined S100A9 protein aided expanded skin regeneration and rescued dermal thinning in rats in vivo as well as increasing ECM deposition during expansion.

Conclusions: These findings demonstrate that mechanical stretch promoted expanded skin regeneration by upregulating S100A9 expression. Our study laid the foundation for clinically improving tissue expansion using S100A9.

背景:在整形外科中,组织扩张被广泛用于修复皮肤缺陷。然而,低膨胀效率和由薄而膨胀的皮肤引起的皮肤破裂仍然是在膨胀过程中促进皮肤再生的重大挑战。S100钙结合蛋白A9(S100A9)在促进伤口愈合中是必需的;然而,它在组织扩张过程中对皮肤再生的影响尚不清楚。本研究的目的是探索S100A9在皮肤再生中的作用,特别是胶原蛋白的产生,以研究其在组织扩张过程中皮肤再生的重要性。方法:研究S100A9及其受体toll样受体4(TLR-4)和晚期糖基化终产物受体在扩张皮肤中的表达和分布。在大鼠和患者的皮肤样本中研究了这些特征。此外,还研究了S100A9在体外拉伸角质形成细胞中的表达。还观察了S100A9对皮肤成纤维细胞增殖和迁移的影响。TAK-242用于抑制S100A9与TLR-4的结合;测定成纤维细胞中I型胶原(COL I)、转化生长因子β(TGF-β)、TLR-4和磷酸化细胞外信号相关激酶1/2(p-ERK1/2)的水平。此外,通过siRNA转染将成纤维细胞与拉伸的S100A9敲除角质形成细胞共培养,并研究成纤维细胞中COL I、TGF-β、TLR-4和p-ERK1/2的水平。此外,还分析了扩张皮肤的面积、真皮厚度以及COL I、TGF-β、TLR-4和p-ERK1/2的合成,以确定S100A9对扩张皮肤的影响。结果:S100A9和TLR-4的表达增加与扩张真皮中细胞外基质(ECM)的减少有关。此外,S100A9通过TLR-4/ERK1/2途径促进人皮肤成纤维细胞的增殖和迁移以及成纤维细胞中COL I和TGF-β的表达。我们发现,机械拉伸诱导的S100A9表达和角质形成细胞的分泌刺激了皮肤成纤维细胞中COL I、TGF-β、TLR-4和p-ERK1/2的表达。重组S100A9蛋白有助于大鼠体内扩大皮肤再生,挽救真皮变薄,并增加扩张过程中ECM的沉积。结论:这些发现表明,机械拉伸通过上调S100A9的表达来促进扩张的皮肤再生。我们的研究为S100A9在临床上改善组织扩张奠定了基础。
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引用次数: 0
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Burns & Trauma
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