Skin is the most external organ of the body, protecting it from environmental factors. The barrier functions of the skin are significantly supported by the cutaneous microbiome (bacteria, fungi, mites and viruses). To perform its functions, the microbiome must have a certain size and diversity. The microbiome balance can be disrupted by internal and environmental factors. Disturbed homoeostasis is observed, among other conditions, in the course of atopic dermatitis, psoriasis, acne vulgaris, rosacea, and seborrhoeic dermatitis. The skin is inhabited primarily by four phyla of bacteria: Actinobacteria, Firmicutes, Bacteroidetes and Proteobacteria. The dominant fungal and mite species residing on the skin are lipophilic fungi of the genus Malassezia and Demodex, respectively. Viruses are an unstable but essential element of the skin microbiome, particularly viruses containing double stranded DNA (dsDNA) such as Polyomaviridae and Papillomaviridae.streszczenie Skóra jest najbardziej zewnętrznym organem ciała, który stanowi ochronę przed czynnikami środowiskowymi. Barierowe funkcje skóry są istotnie wspierane przez jej mikrobiom (bakterie, grzyby, roztocza i wirusy). Mikrobiom, by pełnił swoje funkcje, musi charakteryzować się określoną wielkością i różnorodnością. Czynniki wewnętrzne i środowiskowe mogą zaburzać równowagę mikrobiomu. Zaburzoną homeostazę obserwuje się w przebiegu m.in. atopowego zapalenia skóry, łuszczycy, trądziku pospolitego, trądziku różowatego i łojotokowego zapalenia skóry. Skóra zasiedlana jest głównie przez cztery typy bakterii: Actinobacteria, Firmicutes, Bacteroidetes i Proteobacteria. Najważniejszymi gatunkami grzybów zasiedlających skórę są lipofilne grzyby z rodzaju Malassezia, a roztoczy -nużeńce (Demodex). Wirusy stanowią niestały, ale istotny element mikrobiomu skóry, zwłaszcza wirusy zawierające dwuniciowe DNA (dsDNA), takie jak poliomawirusy (Polyomaviridae) i papillomawirusy (Papillomaviridae).How to cite this article Adamczyk K., Garncarczyk A.A., Antończak P.P.: The microbiome of the skin. Dermatol Rev/Przegl Dermatol 2018, 105, 285-297.
Background:The human skin microbiome is represented by bacteria, fungi, viruses, and mites.Aims: Every human being possess their own unique skin microbiome because intrinsic and environmental factors have a significant impact on the quality and quantity of microorganism. Every site of the body is a separate microbial niche. Patients:The feet are one of the most unique and heterogeneous microbial niches of human body with areas that differ by skin thickness, anatomical features, distribution of sweat glands, pH, and the availability of oxygen.Results: Healthy skin of the foot is inhabited by Corynebacteriaceae, Micrococcaceae,
Background: The skin is a protective barrier of the body against external factors, and its damage leads to a loss of integrity. Normal wound healing results in a correct, flat, bright, and flexible scar. Initial skin damage and patient specific factors in wound healing contribute that many of these scars may progress into widespread or pathologic hypertrophic and keloid scars. The changes in cosmetic appearance, continuing pain, and loss of movement due to contracture or adhesion and persistent pruritis can significantly affect an individual's quality of life and psychological recovery post injury. Many different treatment methods can reduce the trauma and surgical scars. Manual scar treatment includes various techniques of therapy. The most effectiveness is a combined therapy, which has a multidirectional impact. Clinical observations show an effectiveness of manual scar therapy. Material and methods:The aim of this work was to evaluate effectiveness of the scar manual therapy combined with complementary methods on the postoperative scars. Treatment protocol included two therapies during 30 min per week for 8 weeks. Therapy included manual scar manipulation, massage, cupping, dry needling, and taping.Results: Treatment had a significant positive effect to influence pain, pigmentation, pliability, pruritus, surface area, and scar stiffness. Improvement of skin parameters (scar elasticity, thickness, regularity, color) was also noticed. Conclusion:To investigate the most effective manual therapy strategy, further studies are needed, evaluating comparisons of different individual and combined scar therapy modalities.
Introduction. Tranilast (N-(3',4'-demethoxycinnamoyl)-anthranilic acid)is an anti-allergic drug. Its mechanism of action is based on the inhibition of antigen-induced release of chemical mediators from mast cells and basophils. It also reveals antifibroproliferative activities. These properties of tranilast are used in the treatment of hypertrophic scars and keloids. Keloids are characterized by incorrect extracellular matrix components turnover. Fibroblasts derived from keloids reveal overproduction of collagen type I and decreased degradation of extracellular matrix in comparison with normal fibroblasts. Fibroblast activation protein α (FAP-α) may play an important role in remodeling of extracellular matrix and the invasive properties of keloids. Objective. In the present study, the effect of tranilast on expression of FAP-α gene and its protein was evaluated in normal human dermal fibroblasts and fibroblasts derived from keloids cultured in vitro. Materials and methods. In the first stage of the study, the influence of tranilast on cell viability was estimated. The second stage of the study included the quantitative evaluation of FAP-α mRNA expression in normal and keloid fibroblasts treated with tranilast. The third stage of the study comprised fibroblast activation protein α expression analysis in the examined cells treated with tranilast. Results and conclusions. The expression of FAP-α gene and fibroblast activation protein α is higher in keloid fibroblasts. Tranilast at concentrations of 3 μM and 30 μM up-regulated mRNA FAP-α expression in normal fibroblasts but did not influence keloid fibroblasts. The drug, at concentrations of 30 μM and 300 μM up-regulated fibroblast activation protein α expression in normal fibroblasts and did not influence keloid fibroblasts. Tranilast antiproliferative effect is not associated with FAP-α expression in keloid fibroblasts. Original article/Praca oryginalnaThe effect of tranilast on fibroblast activation protein α (FAP-α) expression in normal and keloid fibroblasts in vitro Wpływ tranilastu na ekspresję białka aktywującego fibroblasty α (FAP-α) w fibroblastach prawidłowych oraz fibroblastach keloidowych in vitro
Objective Keloids arise most often as a result of abnormal wound healing. The lesion characterizes inflammation and fibroproliferation. Fibroblast activation protein alpha (FAP‐α) is one of enzymes engaged in keloid formation. It is serine protease that facilitates cells invasion and growth. FAP‐α possess also non‐enzymatic activity and plays role in activation of cell signaling. The aim of the study was to assess the impact of culture conditions on the proliferation of keloid fibroblasts and the expression of FAP‐α. Analysis of utility of 3D models of keloid in in vitro study of pathogenesis of keloids was also made. Methods NHDF and KEL FIB cells were cultured in vitro in 2D cultures and 3D Matrigel models. The viability of cells was assayed spectrophotometrically with WST‐1 test. FAP‐α protein amount in cell cultures and 3D models was evaluated with the use of ELISA test. Results KEL FIB fibroblasts exhibited higher viability than NHDF fibroblasts in all three models of keloid. The expression of FAP‐α is different in normal and keloid fibroblasts. In vitro conditions influence the expression of FAP‐α in NHDF cells but not in KEL FIB cells. Conclusions This preliminary study has shown that the expression of FAP‐α, similarly to other enzymes engaged in keloid formation, is different in keloids in vivo and in in vitro models. FAP‐α expression is modulated by in vitro conditions in normal fibroblasts but not in keloid fibroblasts.
StreSzczenieProcesy naprawcze (reperatywne) uszkodzonych tkanek należą do podstawowych procesów biologicznych zapewniających utrzymanie homeostazy organizmu. Zasadniczo obejmują fazę zapalną, proliferacyjną oraz przebudowy. Końcowym efektem gojenia się uszkodzonych tkanek jest powstanie blizny. Nieprawidłowości w przebiegu gojenia się ran mogą być przyczyną tworzenia keloidów (bliznowców). W patofizjologii keloidów obserwuje się zarówno nieprawidłowości w migracji, proliferacji i apoptozie komórek, jak i w syntezie oraz sekrecji białek, cytokin, enzymów proteolitycznych degradujących składniki macierzy pozakomórkowej, a także ich inhibitorów. Dotychczasowo stosowane terapie nie przynoszą zadowalających efektów kosmetycznych. Obecnie prowadzone badania skupiają się na poszukiwaniu metod bezpośredniego hamowania procesu fibroproliferacyjnego poprzez modulowanie ekspresji cytokin, hamowanie proliferacji fibroblastów oraz regulowanie biosyntezy i degradacji składników macierzy pozakomórkowej. AbStrActReparation of damaged tissues is an essential biological process that ensures maintenance of homeostasis. Basically it includes phases of inflammation, proliferation and remodeling. The result of healing of damaged tissues is scar formation. Abnormalities in the course of wound healing may lead to keloid formation. The pathophysiology of keloids is characterized by improper migration, proliferation and apoptosis of cells as well as imbalanced synthesis and secretion of proteins, cytokines, proteolytic enzymes and their inhibitors. To date, applied therapeutic methods do not lead to satisfactory cosmetic results of the treatment. Current research focuses on developing methods for direct inhibition of the fibroproliferative process, mainly through modulation of cytokine expression and in consequence suppression of fibroblast proliferation and balancing of synthesis and degradation of extracellular matrix components.
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