Significance: A moist wound environment has several benefits that result in faster and better quality of healing. It facilitates autolytic debridement, reduces pain, reduces scarring, activates collagen synthesis, facilitates and promotes keratinocyte migration over the wound surface, and supports the presence and function of nutrients, growth factors, and other soluble mediators in the wound microenvironment. Recent Advances: Wound dressings can be utilized to create, maintain, and control a moist environment for healing. Moist wound dressings can be divided into films, foams, hydrocolloids, hydrogels, and alginates. We are also including negative pressure wound therapy systems in the moist dressings. Critical Issues: An optimal wound dressing should provide a moist environment and have an optimal water vapor transmission rate (WVTR) and absorptive capacity. It should also protect the wound against trauma and contamination and be easy to apply, painless to remove, and esthetically acceptable or even pleasing. Future Directions: Interventions, particularly dressing changes, by medical caregivers are labor intensive and expensive and there should be a continuous effort to reduce their number per week. Smart dressings with integrated microsensors and delivery capabilities that would allow wireless real-time monitoring and treatment of the wound would be very advantageous. This way the state of the wound as well as the wear time of the dressing could be assessed without dressing removal or visit to the wound care center. In addition, an ability to adjust the WVTRs to the exudate level of the wound (or having a large absorptive capacity without changing the WVTR) would be useful. This feature would guarantee an optimal level of hydration of the wound surface throughout the treatment.

Acute and chronic wounds affect millions of people around the world, imposing a growing financial burden on patients and hospitals. Despite the application of current wound management strategies, the physiological healing process is disrupted in many cases, resulting in impaired wound healing. Therefore, more efficient and easy-to-use treatment modalities are needed. In this study, we demonstrate the benefit of in vivo printed, growth factor-eluting adhesive scaffolds for the treatment of full-thickness wounds in a porcine model. A custom-made handheld printer is implemented to finely print gelatin-methacryloyl (GelMA) hydrogel containing vascular endothelial growth factor (VEGF) into the wounds. In vitro and in vivo results show that the in situ GelMA crosslinking induces a strong scaffold adhesion and enables printing on curved surfaces of wet tissues, without the need for any sutures. The scaffold is further shown to offer a sustained release of VEGF, enhancing the migration of endothelial cells in vitro. Histological analyses demonstrate that the administration of the VEGF-eluting GelMA scaffolds that remain adherent to the wound bed significantly improves the quality of healing in porcine wounds. The introduced in vivo printing strategy for wound healing applications is translational and convenient to use in any place, such as an operating room, and does not require expensive bioprinters or imaging modalities.

Objective: There is an unmet need to improve immediate burn care, particularly when definitive treatment is delayed. Therefore, the purpose of this project was to formulate a hydrogel that contains very high concentrations of antibiotics and validate its use together with a platform wound device (PWD) for the immediate care of burns. Approach: The hydrogel properties were optimized by using a rheometer, differential scanning calorimetry, and liquid chromatography–mass spectrometry and were tested in an infected porcine burn model. Immediately, after burn creation, the burns were infected with different bacteria. Subsequently, the burns infected with Staphylococcus aureus , Pseudomonas aeruginosa , and Acinetobacter baumannii were covered with the PWD and treated with a single dose of hydrogel containing 1000 × minimum inhibitory concentration of vancomycin, gentamicin, and minocycline, respectively. On day 7 or 45, the animals were euthanized, and the burns were harvested for histology and quantitative bacteriology. Results: 0.625% was the best alginate concentration for the hydrogel in terms of viscosity, stability, and drug release. The porcine studies demonstrated that vancomycin-, gentamicin-, and minocycline-treated tissues contained significantly less bacteria and reduced depth of tissue necrosis in comparison to controls. Innovation: The PWD represents a platform technology that begins at the point of the first treatment by protecting the wound and allowing administration of topical therapeutics. The device can be adapted to enclose any size burn over any contour of the body. Conclusion: Antibiotics can be delivered safely in very high concentrations in a hydrogel using the PWD, and burn infections can be treated successfully with this method.

Significance: Negative pressure wound therapy (NPWT) has been in practice for decades, proving its utility in many applications, ranging from acutely infected wounds to complex combat wounds and skin grafting. It has been routinely demonstrated that NPWT has superior wound healing outcomes compared with previous standard-of-care therapies. However, the technique involves some challenges related to each of the components that comprise the therapy. The purpose of this article is to highlight the challenges, introduce the recent advancements, and discuss about the future directions in NPWT systems. Recent Advances: New techniques and materials have been developed to improve the currently used NPWT systems with promising results when utilized with appropriate indications. Many advancements have been introduced in modes of negative pressure delivery, pumps, interface dressings, adhesive dressings, and tubing technology. Critical Issues: An optimal NPWT system would avoid the common problems such as failure to deliver negative pressure due to loss of an airtight seal or tissue ingrowth into the interface dressing causing painful dressing changes and bleeding. Other challenges include infection control and patient pain and discomfort that may contribute to noncompliance. Future Directions: Many studies have been performed to evaluate the optimal combination of settings and components in various wounds; however, there is still no clear “best” answer for many specific patient-wound scenarios. Novel and emerging tissue engineering and regenerative medicine approaches could potentially be utilized in the future NPWT systems and thus, this review will discuss some novel ideas for future considerations.

CCHCR1 (Coiled-Coil α-Helical Rod protein 1) is a putative psoriasis candidate gene with the risk alleles CCHCR1*WWCC and *Iso3, the latter inhibiting the translation of isoform 1. CCHCR1 was recently shown to be a centrosomal protein, as well as a component of cytoplasmic processing bodies (P-bodies) that regulate mRNA turnover. The function of CCHCR1 has remained unsettled, partly because of the inconsistent findings; it has been shown to play a wide variety of roles in divergent processes, e.g., cell proliferation and steroidogenesis. Here we utilized RNA sequencing (RNAseq) using HEK293 cells overexpressing isoforms 1 or 3 (Iso1, Iso3 cells), in combination with the coding non-risk or risk (*WWCC) haplotype of CCHCR1. Our aim was to study the overall role of CCHCR1 and the effects of its variants. The overexpression of CCHCR1 variants in HEK293 cells resulted in cell line-specific expression profiles though several similarities were observable. Overall the Iso1 and Iso3 cells showed a clear isoform-specific clustering as two separate groups, and the Non-risk and Risk cells often exhibited opposite effects. The RNAseq supported a role for CCHCR1 in the centrosomes and P-bodies; the most highlighted pathways included regulation of cytoskeleton, adherens and tight junctions, mRNA surveillance and RNA transport. Interestingly, both the RNAseq and immunofluorescent localization revealed variant-specific differences for CCHCR1 within the P-bodies. CCHCR1 influenced a wide variety of signaling pathways, which could reflect its active role in the P-bodies and centrosomes that both are linked to the cytoskeleton; as a centrosomal P-body protein CCHCR1 may regulate diverse cytoskeleton-mediated functions, such as cell adhesion and -division. The present findings may explain the previous inconsistent observations about the functions of CCHCR1.

Background: Wound infection can impair postoperative healing. Topical antibiotics have potential to treat wound infection and inflammation and minimize the adverse effects associated with systemic antibiotics. Methods: Full-thickness porcine wounds were infected with Staphylococcus aureus. Using polyurethane wound enclosure devices, wounds were treated with topical 100 μg/ml minocycline, topical 1000 μg/ml minocycline, topical saline control, or 4 mg/kg intravenous minocycline. Bacteria were quantified in wound tissue and fluid obtained over 9 hours. Immunosorbent assays were used to analyze inflammatory marker concentrations. Minocycline’s effect on in vitro migration and proliferation of human keratinocytes and fibroblasts was tested using scratch assays and metabolic assays, respectively. Results: After 6 hours, 100 and 1000 μg/ml topical minocycline decreased bacteria in wound tissue to 3.5 ± 0.87 and 2.9 ± 2.3 log colony-forming units/g respectively, compared to 8.3 ± 0.9 log colony-forming units/g in control wounds (p < 0.001) and 6.9 ± 0.2 log colony-forming units/g in wounds treated with 4 mg/kg intravenous minocycline (p < 0.01). After 2 hours, topical minocycline reduced concentrations of the inflammatory cytokines interleukin-1β, interleukin-6, and tumor necrosis factor-α (p < 0.01), and inflammatory cell counts in wound tissue (p < 0.05). In noninfected wounds, topical minocycline significantly reduced interleukin-1β, interleukin-6, and inflammatory cell counts after 4 hours (p < 0.01). Matrix metalloproteinase-9 concentrations decreased after 1-hour treatment (p < 0.05). Keratinocyte and fibroblast in vitro functions were not adversely affected by 10 μg/ml minocycline or less. Conclusions: Topical minocycline significantly reduces bacterial burden and inflammation in infected wounds compared with wounds treated with intravenous minocycline or control wounds. Minocycline also decreases local inflammation independently of its antimicrobial effect.