Introduction: It has been suggested that wound ischemia is involved in the promotion of bacterial proliferation, which is a detrimental factor in wound healing. Increasing evidence from clinical data suggests that bacteria live within biofilms on nonhealing wounds. Yet, there have been no reports clarifying the contribution of wound ischemia to biofilm formation on nonhealing wounds. Objectives: The present study addresses the question of how ischemia affects biofilm formation at wound sites. Methods: Standardized dorsal ischemic flaps were lifted and sutured on the backs of Sprague–Dawley rats. Partial thickness wounds were created on these flaps, and a suspension of Pseudomonas aeruginosa was applied to each wound. We analyzed wound exudate, histological findings, and biofilm formation. Results: The quantities of exudate from the wounds on the ischemic flaps were greater than those from control wounds. Surprisingly, in ischemic wounds, biofilm formation was diminished and leukocyte infiltration was decreased. Conclusion: Our findings demonstrate for the first time that the ischemic condition may not contribute to the development of biofilm formation on skin wounds through regulating leukocytic responses.
Background Since the Mozart effect was first reported in 1993, it has been commonly proposed that listening to music has beneficial effects on physical and mental health. The putative relaxation effect of Mozart's music has been exploited for commercial purposes. Moreover, it has been reported that Bach's music has a relaxation similar to Mozart's music. Despite these widespread claims, few scientific or clinical investigations have shown compelling evidence demonstrating relaxation effects of Mozart's and/or Bach's music. Objective The purpose of this study was to evaluate the effects of Mozart's Sonata for Four Hands in D‐major (K448) and Bach's Brandenburg Concerto No.4 in G‐major (BWV1049) on heart rate (HR), blood pressure (BP), and autonomic nervous activity in healthy young adults. Methods We enrolled seventeen healthy young adults with an average age of 21.9 ± 0.9 years in our study. After 10 minutes of rest, all volunteers underwent three tasks in a randomized order: an examination to induce a mental work load and two 8‐minute intervals of music listening. The control group underwent two 8‐minute periods of silence rather than music. We assessed the electrocardiogram continuously from the start of each experiment to completion. Spectral analysis was performed to determine the low frequency (LF, 0.04–0.15 Hz) and high frequency (HF, 0.15–0.40 Hz) spectral components of heart late variability (HRV). The HF component was used as an index of parasympathetic nervous activity, and the ratio of LF to HF components (LF/HF) was used as an index of sympathetic nervous activity. Additionally, we measured BP before and after each workload‐inducing examination, and after each music‐listening or silence period. The selected music consisted of K448 and BWV1049. All data are expressed as mean ± SE. One‐way repeated‐measures ANOVA and multiple comparison tests were performed to compare each index. A value of P < 0.05 was considered significant. Results There were significant decrease in HR and diastolic blood pressure (DBP) upon listening to K448 and BWV1049, or during silence in the case of control, but no significant change in systolic blood pressure (SBP) in any condition. HF spectral components of HRV showed insignificant changes in BWV1049 and control; however, it was significantly decreased in K448. LF/HF was not significantly lower after the examination compared to other task conditions in the K448, BWV1049, or control groups. There were no significant differences in the rate of change in HR, SBP, DBP, HF, and LF/HF during K448, BWV1049, or silence (control). Conclusion We did not identify significant changes in HR, BP, or LF/HF in healthy young adults while they listened to K448 or BWV1049. However, HF did decrease after listening to K448. Overall, our findings suggested that Mozart's and Bach's music yielded little relaxation effect as indicated HR, BP, and autonomic nervous activity. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .
Abstract Low‐energy extracorporeal shock wave ( LE ‐ ESW ) treatment has been shown to accelerate wound repair; however, the mechanisms of treatment remain unclear. In the present study, we addressed the role of endothelial nitric oxide synthase ( eNOS ). A single LE ‐ ESW treatment accelerated the healing of wounds in diabetic mice caused by the injection of streptozotocin. This accelerated healing was accompanied by the increased expression of eNOS and vascular endothelial growth factor ( VEGF ) and the generation of new vessels at the wound tissues. These results raised the possibility that eNOS may be involved in the beneficial effects of LE ‐ ESW treatment. To address this possibility, we compared the effects of this treatment between mice with a genetic disruption of eNOS knockout ( eNOS‐KO mice) and wild‐type ( WT ) control mice. Interestingly, the LE ‐ ESW ‐induced acceleration of wound closure and the increase in VEGF expression and neovascularization was significantly attenuated in eNOS‐KO mice compared with WT mice. Considered collectively, these results showed that eNOS was induced at the wound tissues by LE ‐ ESW treatment and played a critical role in the therapeutic effects of this treatment by accelerating the wound healing by promoting VEGF expression and neovascularization.
Tumor necrosis factor (TNF)-α is quickly released and initiates inflammation at wound tissues, but its precise role in wound healing is not fully understood. We examined the contribution of this cytokine to the early process of healing using a mouse model with full-thickness wounds in skin. TNF-α synthesis was detected just after wound creation, increased during the first several hours, reached a peak level on day 1, and then decreased to the basal level. In mice treated with anti-TNF-α mAb, wound closure was significantly delayed, and distances between the panniculus carnosus edges were significantly longer on day 3, compared with control. Inflammatory cell and fibroblast density were markedly decreased on day 3 in the anti-TNF-α mAb-treated mice compared with control. In contrast, wound healing was accelerated on day 3 when mice were treated with bioactive TNF-α. These results indicate that TNF-α is involved in the early process of wound healing.
The gene encoding the periplasmic beta-N-acetylglucosaminidase (GlcNAcase B) from a marine Alteromonas sp. strain, O-7, was cloned and sequenced. The protein sequence of GlcNAcase B revealed a highly significant homology with Vibrio GlcNAcase and alpha- and beta-chains of human beta-hexosaminidase.
Interferon (IFN)-γ is mainly secreted by CD4+ T helper 1 (Th1), natural killer (NK) and NKT cells after skin injury. Although IFN-γ is well known regarding its inhibitory effects on collagen synthesis by fibroblasts in vitro, information is limited regarding its role in wound healing in vivo. In the present study, we analyzed how the defect of IFN-γ affects wound healing. Full-thickness wounds were created on the backs of wild type (WT) C57BL/6 and IFN-γ-deficient (KO) mice. We analyzed the percent wound closure, wound breaking strength, accumulation of leukocytes, and expression levels of COL1A1, COL3A1, and matrix metalloproteinases (MMPs). IFN-γKO mice exhibited significant attenuation in wound closure on Day 10 and wound breaking strength on Day 14 after wound creation, characteristics that are associated with prolonged neutrophil accumulation. Expression levels of COL1A1 and COL3A1 mRNA were lower in IFN-γKO than in WT mice, whereas expression levels of MMP-2 (gelatinase) mRNA were significantly greater in IFN-γKO than in WT mice. Moreover, under neutropenic conditions created with anti-Gr-1 monoclonal antibodies, wound closure in IFN-γKO mice was recovered through low MMP-2 expression levels. These results suggest that IFN-γ may be involved in the proliferation and maturation stages of wound healing through the regulation of neutrophilic inflammatory responses.
Cryptococcus neoformans is an opportunistic fungal pathogen and the causative agent of the disease cryptococcosis. Cryptococcosis is initiated as a pulmonary infection and in conditions of immune deficiency disseminates to the blood stream and central nervous system, resulting in life-threatening meningoencephalitis. A number of studies have focused on the development of a vaccine against Cryptococcus, primarily utilizing protein-conjugated components of the Cryptococcus polysaccharide capsule as antigen. However, there is currently no vaccine against Cryptococcus in the clinic. Previous studies have shown that the glycosphingolipid, glucosylceramide (GlcCer), is a virulence factor in C. neoformans and antibodies against this lipid inhibit fungal growth and cell division. In the present study, we have investigated the possibility of using GlcCer as a therapeutic agent against C. neoformans infections in mouse models of cryptococcosis. GlcCer purified from a non-pathogenic fungus, Candida utilis, was administered intraperitoneally, prior to infecting mice with a lethal dose of C. neoformans. GlcCer administration prevented the dissemination of C. neoformans from the lungs to the brain and led to 60% mouse survival. GlcCer administration did not cause hepatic injury and elicited an anti-GlcCer antibody response, which was observed independent of the route of administration and the strains of mouse. Taken together, our results suggest that fungal GlcCer can protect mice against lethal doses of C. neoformans infection and can provide a viable vaccination strategy against Cryptococcus.
The cell walls and capsules of Cryptococcus neoformans , a yeast-type fungal pathogen, are rich in polysaccharides. Dectin-2 is a C-type lectin receptor (CLR) that recognizes high-mannose polysaccharides.
