A 3D In Vitro Model for Burn Wounds: Monitoring of Regeneration on the Epidermal Level.
Ontology highlight
ABSTRACT:
SUBMITTER: Schneider V
PROVIDER: S-EPMC8466997 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Background: An experimental study was undertaken to determine the efficacy of the epidermal growth factor (EGF) with tocotrienol-rich fraction (TRF) cream in the wound-healing process on skin with deep partial-thickness burn in rats. Methods: A total of 180 Sprague-Dawley rats were randomly divided into six groups of six each and were: untreated control, treated with Silverdin® cream, base cream, base cream with c% EGF, base cream with 3% TRF or base cream with c% EGF and 3% TRF, respectively. Creams were applied once daily for 21 consecutive days. Six animals from each group were sacrificed using anaesthetic overdose on the third, seventh, 11th, 14th and 21st day post-burn. Skin tissues with the wound to be examined were excised for macroscopic and microscopic evaluation and biochemical analyses. Results: EGF + TRF formulation decreased the number of neutrophils, lymphocytes and myofibroblasts post-burn. However, no effects on the number of adipose cells in the healing process were recorded. In addition, lipid peroxidation and nitrite production were found to be reduced post-burn, reducing oxidative stress. Conclusions: Results of the present study indicate that the addition of EGF with TRF have ameliorating effects on deep-partial thickness burn healing parameters.
| S-EPMC7070471 | biostudies-literature
Project description:We used a modified Walker-Mason scald burn rat model to demonstrate that Pseudomonas aeruginosa, a common opportunistic pathogen in the burn ward and notable biofilm former, establishes biofilms within deep partial-thickness burn wounds in rats.Deep partial-thickness burn wounds, ~10% of the TBSA, were created in anesthetized male Sprague-Dawley rats (350-450 g; n = 84). Immediately post-burn, 100 µl of P. aeruginosa in phosphate-buffered saline at 1 × 103, 1 × 104, or 1 × 105 cells/wound was spread over the burn surface . At 1, 3, 7, and 11 days post-burn, animals were euthanized and blood and tissue were collected for complete blood counts, colony-forming unit (CFU) counts, biofilm gene expression, histology, scanning electron microscopy (SEM), and myeloperoxidase activity in the burn eschar.P. aeruginosa developed robust biofilm wound infections, plateauing at ~1 × 109 CFU/g burn tissue within 7 days regardless of inoculum size. Expression of Pseudomonas alginate genes and other virulence factors in the infected wound indicated formation of mature P. aeruginosa biofilm within the burn eschar. Compared to un-inoculated wounds, P. aeruginosa infection caused both local and systemic immune responses demonstrated by changes in systemic neutrophil counts, histology, and myeloperoxidase activity within the burn wound. Additionally, SEM showed P. aeruginosa enmeshed within an extracellular matrix on the burn surface as well as penetrating 500-600 µm deep into the eschar.P. aeruginosa establishes biofilms within deep partial-thickness burn wounds and invades deep into the burned tissue. This new in vivo biofilm infection model is valuable for testing novel anti-biofilm agents to advance burn care.
| S-EPMC6300396 | biostudies-literature
Project description:INTRODUCTION:The prognosis for severe burns has improved significantly over the past 50 years. Meanwhile, burns have become an affliction mainly affecting the less well-developed regions of the world. Early excision and skin grafting has led to major improvements in therapeutic outcomes. AREAS COVERED:The purpose of this article is to survey the use of pharmacotherapy to treat different pathophysiological complications of burn injury. The author, herein, discusses the use of drug treatments for a number of systemic metabolic disturbances including hyperglycemia, elevated catabolism, and gluconeogenesis. EXPERT OPINION:Advancements in personalized and molecular medicine will make an impact on burn therapy. Similarities between severe burns and other critically ill patients will lead to cross-fertilization between different medical specialties. Furthermore, advances in stem cells and tissue regeneration will lead to improved healing and less lifelong disability. Indeed, research in new drug therapy for burns is actively progressing for many different complications.
| S-EPMC6364296 | biostudies-literature
Project description:SIGNIFICANCE:Research in tissue engineering and in vitro organ formation has recently intensified. To assess tissue morphology, the method of choice today is restricted primarily to histology. Thus novel tools are required to enable noninvasive, and preferably label-free, three-dimensional imaging that is more compatible with futuristic organ-on-a-chip models. AIM:We investigate the potential for using multiphoton microscopy (MPM) as a label-free in vitro approach to monitor calcium-induced epidermal differentiation. APPROACH:In vitro epidermis was cultured at the air-liquid interface in varying calcium concentrations. Morphology and tissue architecture were investigated using MPM based on visualizing cellular autofluorescence. RESULTS:Distinct morphologies corresponding to epidermal differentiation were observed. In addition, Ca2??+??-induced effects could be distinguished based on the architectural differences in stratification in the tissue cultures. CONCLUSIONS:Our study shows that MPM based on cellular autofluorescence enables visualization of Ca2??+??-induced differentiation in epidermal skin models in vitro. The technique has potential to be further adapted as a noninvasive, label-free, and real-time tool to monitor tissue regeneration and organ formation in vitro.
| S-EPMC7210787 | biostudies-literature
Project description:The interaction of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor inducible 14 (Fn14) participates in inflammatory responses, fibrosis, and tissue remodeling, which are central in the repair processes of wounds. Fn14 is expressed in main skin cells including dermal fibroblasts. This study was designed to explore the therapeutic effect of TWEAK on experimental burn wounds and the relevant mechanism underlying such function. Third-degree burns were introduced in two BALB/c mouse strains. Recombinant TWEAK was administrated topically, followed by the evaluation of wound areas and histologic changes. Accordingly, the downstream cytokines, inflammatory cell infiltration, and extracellular matrix synthesis were examined in lesional tissue. Moreover, the differentiation markers were analyzed in cultured human dermal fibroblasts upon TWEAK stimulation. The results showed that topical TWEAK accelerated the healing of burn wounds in wild-type mice but not in Fn14-deficient mice. TWEAK strengthened inflammatory cell infiltration, and exaggerated the production of growth factor and extracellular matrix components in wound areas of wild-type mice. Moreover, TWEAK/Fn14 activation elevated the expression of myofibroblastic differentiation markers, including alpha-smooth muscle actin and palladin, in cultured dermal fibroblasts. Therefore, topical TWEAK exhibits therapeutic effect on experimental burn wounds through favoring regional inflammation, cytokine production, and extracellular matrix synthesis. TWEAK/Fn14 activation induces the myofibroblastic differentiation of dermal fibroblasts, partially contributing to the healing of burn wounds.
| S-EPMC6021523 | biostudies-literature
Project description:ObjectiveA burn is an inflammatory injury to the skin or other tissue due to contact with thermal, radioactive, electric, or chemical agents. Burn injury is an important cause of disability and death worldwide. Obesity is a significant public health problem, often causing underlying systemic inflammation. Studying the combined impact of burn injuries on obese patients has become critical to the successful treatment of these patients. The aim of this paper is to highlight the effect of inflammation associated with burn injuries on several body weight group in a rat study.Materials and methodsDifferent degrees of obesity and burns were established in rats and divided into a normal weight group, overweight group, obese group, second-degree burn group, third-degree burn group, over-weight second-degree burn group, over-weight third-degree burn group, obese second-degree burn group, and obese third-degree burn group (20 rats per group). Changes in inflammatory factors and growth factor were measured on the 1st, 3rd, 7th and 14th days after burns were inflicted.ResultsThe ELISA test showed that in the unburned control group, MCP-1, IL-1β and TNF-α protein expressions in the obese and over-weight groups were higher than the normal-weight group (P < 0.05). RT-PCR test showed that the expressions of MCP-1, IL-1β and TNF-α genes in the obese group were higher compared to the overweight and normal weight groups (P < 0.05). Three and 7 days after burns were inflicted, the level of VEGF in the normal weight group was higher than the obese group (P < 0.05), however increased VEGF was not observed on days 1 and 14.ConclusionBurn injury and obesity have a mutually synergistic effect on the body's inflammatory response.
| S-EPMC7731656 | biostudies-literature
Project description:This paper describes the experimental setup and measurements of the emissivity of porcine skin samples over the band of 80-100 GHz. Measurements were conducted on samples with and without dressing materials and before and after the application of localized heat treatments. Experimental measurements indicate that the differences in the mean emissivity values between unburned skin and burned damaged skin was up to ~0.28, with an experimental measurement uncertainty of ±0.005. Measured differences in the mean emissivity values between unburned and burn damaged skin increases with the depth of the burn, indicating a possible non-contact technique for assessing the degree of a burn. The mean emissivity of the dressed burned skin was found to be slightly higher than the undressed burned skin, typically ~0.01 to ~0.02 higher. This indicates that the signature of the burn caused by the application of localized heat treatments is observable through dressing materials. These findings reveal that radiometry, as a non-contact method, is capable of distinguishing between normal and burn-damaged skin under dressing materials without their often-painful removal. This indicates the potential of using millimeter wave (MMW) radiometry as a new type of medical diagnostic to monitor burn wounds.
| S-EPMC6651191 | biostudies-literature
Project description:Secondary burn necrosis is the expansion and deepening of the original burn injury several days after injury. Limiting the extent of secondary burn necrosis may improve outcomes. In this study, we examined the ability of the lipid mediator of inflammation-resolution resolvin D2 (RvD2) and chromatin-lysing enzyme (DNase) to reduce secondary burn necrosis. Male Wistar rats were injured using a brass comb with 4 prongs heated in boiling water. This method created 2 parallel rows of 4 rectangular burned areas separated by 3 unburned interspaces. Starting at 2 hours after the burn injury, rats received either 25 ng/kg RvD2 intravenously daily for 7 days or 200 U/kg DNase every 12 hours for 3 days. We documented the necrosis around the initial wounds by digital photography. We used laser Doppler to assess the total blood flux in the burn area. We evaluated the functionality of the capillary network in the interspaces by optical coherence tomography angiography. We performed histological examination of wound skin tissue samples collected at 14 days postburn. We found that the interspace areas were preserved and had higher blood flow in the RvD2-treated group, while the burn areas expanded into the interspace areas, which were confluent by 7 days postburn, in the control-untreated group. We found a larger monocyte-to-neutrophil ratio in the RvD2-treated group compared with the DNase-treated and control groups (P < .05). Overall, RvD2 suppresses secondary necrosis and starts regeneration, highlighting the role of inflammation resolution as a potential therapeutic target in burn care.
| S-EPMC5832489 | biostudies-literature
Project description:At present, enzyme debridement preparation has shown a good curative effect on eschar removal of burn wounds. Keratinase has shown great potential in enzymatic debridement because of its good fibrin-degrading ability. In this study, the debridement of keratinase was examined by using a third degree burn wound model in rats. We observed the wound, and keratinase shortened the time of eschar dissolution after debridement. Histopathology and immunofluorescence staining showed that the eschar in the keratinase group became thinner, inflammatory cell infiltration in the wound increased, the fluorescence intensity of the macrophage surface marker CD68 increased, and the CD163/CD86 ratio increased. In bone marrow-derived macrophages (BMDMs), there was no significant difference in the activity of CCK-8 in cells in the keratinase group compared with the control group. The fluorescence intensity of the keratinase group was higher than that of the control group. At 12 h, the cell scratches were obviously closed. The number of migrated Transwell cells increased. Flow cytometry and immunofluorescence analysis showed increased expression of CD206 and Arg-1 and decreased expression of CD86 and iNOS. The gene expression of the Arg-1, iNOS and IL-10 was increased, as shown by qPCR. The secretion of IL-10 was increased and TNF-α was decreased, as shown by ELISA. We concluded that keratinase dissolution of eschar not only has a hydrolytic effect on eschar but may also affect immune regulation to enhance the migration and phagocytosis of macrophages, promote the polarization of macrophages, and further enhance the effect of eschar dissolution. Therefore, keratinase may have good prospects for the debridement of burn wounds.
| S-EPMC10425458 | biostudies-literature
Project description:Cornification and epidermal barrier defects are associated with a number of clinically diverse skin disorders. However, a suitable in vitro model for studying normal barrier function and barrier defects is still lacking. Here, we demonstrate the generation of human epidermal equivalents (HEEs) from human embryonic stem cells (hESCs) and induced pluripotent stem cells (iPSCs). HEEs are structurally similar to native epidermis, with a functional permeability barrier. We exposed a pure population of hESC/iPSC-derived keratinocytes, whose transcriptome corresponds to the gene signature of normal primary human keratinocytes (NHKs), to a sequential high-to-low humidity environment in an air/liquid interface culture. The resulting HEEs had all of the cellular strata of the human epidermis, with skin barrier properties similar to those of normal skin. Such HEEs generated from disease-specific iPSCs will be an invaluable tool not only for dissecting molecular mechanisms that lead to epidermal barrier defects but also for drug development and screening.
| S-EPMC4050479 | biostudies-literature