Search

Diallyl disulfide (DADS) is a garlic (Allium sativum) derived potent anti-inflammatory compound. Due to poor bioavailability, its biological application has limitations. Nanoencapsulation of therapeutic drugs is a promising approach to increase their bioavailability, specificity, and efficacy. In our approach, DADS was coated with the natural polymers alginate and chitosan into a polyelectrolytic nano-formulation. Characterization of the nanoparticles showed monodispersed nanosized particles and a release study at pH 5.5 revealed sustained release of the drug. To investigate the anti-inflammatory efficacy of the DADS nanoparticle (DADS-NP), a comparative study with the free drug was conducted on a mouse model of 12-O-tetradecanoylphorbol-13-acetate (TPA) induced ear edema. The results indicated that DADS-NP significantly alleviated TPA-induced ear edema more effectively than the free drug of the same concentration. Further, mechanistic studies indicated that DADS-NP more efficiently downregulated the phosphorylation of p38 mitogen activated protein kinase which subsequently restricted the activation and nuclear translocation of downstream transcription factor nuclear factor- кB (NF-кB). This downregulated the expression of pro-inflammatory proteins cyclooxygenase-2 (COX-2) and inducible-nitric oxide synthase (i-NOS) thus mitigating ear edema. Cellular internalization of the DADS-NP was observed. Collectively, our studies indicate enhanced anti-inflammatory efficiency of DADS-NP when compared to free DADS suggesting enhanced stability and bioavailability.

Herpesvirus infections of sturgeon pose a potential threat to sturgeon culture efforts worldwide. A new epitheliotropic herpesvirus named Acipenser herpesvirus 3 (AciHV-3) was detected in hatchery-reared Lake Sturgeon Acipenser fulvescens displaying skin lesions in central Canada. The growths were discovered in the fall, reached average prevalence levels of 0.2–40% and eventually regressed. No unusual mortality was observed. The cellular changes within the lesions included epithelial hyperplasia and were reminiscent of other herpesvirus infections. The virus was not evident in lesions examined by electron microscopy. Skin tissue homogenates from symptomatic sturgeon produced atypical cytopathic effects on a primary Lake Sturgeon cell line, and next-generation sequence analysis of the DNA samples revealed the presence of an alloherpesvirus. A new genotyping PCR assay targeting the major capsid protein sequence detected AciHV-3 in symptomatic Lake Sturgeon as well as other apparently healthy sturgeon species. Bayesian inference of phylogeny reconstructed with a concatenation of five alloherpesvirus core proteins revealed a new Alloherpesviridae lineage isomorphic with a new genus. The presence of AciHV-3 homologs in cell lines and sturgeon sequence datasets, low sequence divergence among these homologs and branching patterns within the genotyping phylogeny provide preliminary evidence of an endogenous virus lifestyle established in an ancestral sturgeon. [ABSTRACT FROM AUTHOR]

Psoriasis is a common chronic disease, and existing treatment regimens often exhibit certain toxicities and side effects. Zerumbone (Zer) may possess therapeutic effect, and the objective of this study is to investigate the effect of Zer on psoriasis. A mouse model of psoriasis was established using imiquimod cream, and the role of Zer on the pathological alterations in psoriatic mouse skin was evaluated by psoriasis area and severity index (PASI) score; the effect of Zer on keratinocyte proliferation was evaluated via hematoxylin and eosin staining, Zen image analysis, and immunofluorescence; Immunohistochemistry and enzyme-linked immunoassay were used to evaluate the effect of Zer on tissue inflammatory responses, while malondialdehyde (MDA) and glutathione (GSH) levels were measured to elucidate the role of Zer in modulating oxidative stress; the signaling pathway regulated by Zer was evaluated by western blotting. The results demonstrated that Zer could alleviate the pathological manifestations of psoriasis, reduce PASI score, reduce skin pathological damage and epidermal hyperplasia, diminish the number of CD8+ T cells and cytokine expression levels, decrease the level of MDA and GSH and increase the expression of Nrf and HO-1. Zer was found to regulate the NLRP3/nuclear factor-kappa B (NF-κB) signaling pathway. In conclusion, Zer ameliorated the symptoms of psoriasis in mice, suppressed the keratinocyte hyperproliferation, and mitigates inflammation and oxidative stress in psoriatic skin tissue by regulating the NLRP3/NF-κB pathway. [ABSTRACT FROM AUTHOR]

Khairuddin Djawad,1 Irawan Yusuf,2 Upik Anderiani Miskad,3 Ilhamjaya Jaya Patellongi,4 Muhammad Nasrum Massi5 1Department of Dermatology and Venereology, Hasanuddin University, Makassar, South Sulawesi, Indonesia; 2Department of Pathological Anatomy, Hasanuddin University, Makassar, South Sulawesi, Indonesia; 3Department of Physiology and Biostatics, Hasanuddin University, Makassar, South Sulawesi, Indonesia; 4Department of Physiology, Hasanuddin University, Makassar, South Sulawesi, Indonesia; 5Department of Medical Microbiology, Hasanuddin University, Makassar, South Sulawesi, IndonesiaCorrespondence: Khairuddin Djawad, Email duddin@ymail.comBackground: Ultraviolet B (UVB) exposure leads to formation of photoproducts leading to cellular damage. Prevention using sunscreen can sometimes be inadequate and can be an economic burden. Recent studies have suggested the photoprotective effect of curcumin.Objective: To examine the acute and chronic photoprotective effect of topical curcumin, using cyclobutyl pyrimidine dimers (CPD) and 8-hydroxy2ʹdeoxyguanosine (8-OHdG) expression as markers of DNA-induced damage, and epidermal hyperplasia on UVB-induced mice.Methods: Three treatment groups were established. Group A (negative control) consisted of 5 mice, Group B and C were further divided into two categories to assess acute and chronic effects of topical curcumin and UVB radiation. Each consisted of six subgroups of five mice. Subgroup 1; UVB exposure only (positive control) subgroup 2; acetone and UVB exposure, subgroup 3– 6; topical curcumin application of 100nM, 1μM, 10μM, and 100μM concentrations, respectively. In Group C, there were two categories that received 3x/week UVB exposure for three weeks which effects were being observed at 24 hours and 10 days after the last exposure. The topical curcumin dose was 2mg/mL/cm2 applied 30 minutes prior to 343mJ/cm2/day UVB irradiation. Skin biopsy was done one hour after the last UVB exposure for immunohistochemical and histopathology examinations.Results: Topical curcumin showed a limited yet robust protective effect against CPD and 8-OHdG expression in Group B, while in Group C all concentrations showed significant CPD and 8-OHdG inhibition after 10 days of UVB exposure. The 10μM and 100μM concentrations showed the best epidermal hyperplasia inhibition effect (p< 0.05). No significant differences were found in terms in efficacy either in single nor daily application.Conclusion: Topical curcumin can prevent the formation of the photoproducts CPD and 8-OHdG and epidermal hyperplasia in both acute and chronic exposure in UVB-induced mice.Keywords: curcumin, cyclobutyl pyrimidine dimers, 8-hydroxy2ʹdeoxyguanosine, epidermal hyperplasia, ultraviolet B, UVB, CPD

Immune checkpoint inhibitors (ICIs) have revolutionized cancer therapy. However, structured knowledge to mitigate a patient's specific risk of developing adverse events are limited. Nevertheless, there is an exponential growth of clinical studies combining conventional therapies such as radiation therapy (RT) with ICIs. Cutaneous reactions are among the most common adverse events after monotherapy with either ICIs or RT. So far, little is known about interindividual differences for the risk of developing severe tissue toxicity after the combination of RT with ICIs, and the underlying biological mechanisms are ill defined. We used experimental models of RT‐induced skin injury to analyze skin toxicity after simultaneous application of ICIs. We compared different RT regimens such as fractionated or stereotactic RT with varying dose intensity. Strikingly, we found that simultaneous application of RT and ICIs did not significantly aggravate acute skin injury in two different mouse strains. Detailed examination of long‐term tissue damage of the skin revealed similar signs of epidermal hyperplasia, dermal fibrosis, and adnexal atrophy. In summary, we here present the first experimental study demonstrating the excellent safety profiles of concurrent treatment with RT and ICIs. These findings will help to interpret the development of adverse events of the skin after radioimmunotherapy and guide the design of new clinical trials and clinical decision‐making in individual cases. © 2022 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. [ABSTRACT FROM AUTHOR]

Herpesvirus infections of sturgeon pose a potential threat to sturgeon culture efforts worldwide. A new epitheliotropic herpesvirus named Acipenser herpesvirus 3 (AciHV-3) was detected in hatchery-reared Lake Sturgeon Acipenser fulvescens displaying skin lesions in central Canada. The growths were discovered in the fall, reached average prevalence levels of 0.2–40% and eventually regressed. No unusual mortality was observed. The cellular changes within the lesions included epithelial hyperplasia and were reminiscent of other herpesvirus infections. The virus was not evident in lesions examined by electron microscopy. Skin tissue homogenates from symptomatic sturgeon produced atypical cytopathic effects on a primary Lake Sturgeon cell line, and next-generation sequence analysis of the DNA samples revealed the presence of an alloherpesvirus. A new genotyping PCR assay targeting the major capsid protein sequence detected AciHV-3 in symptomatic Lake Sturgeon as well as other apparently healthy sturgeon species. Bayesian inference of phylogeny reconstructed with a concatenation of five alloherpesvirus core proteins revealed a new Alloherpesviridae lineage isomorphic with a new genus. The presence of AciHV-3 homologs in cell lines and sturgeon sequence datasets, low sequence divergence among these homologs and branching patterns within the genotyping phylogeny provide preliminary evidence of an endogenous virus lifestyle established in an ancestral sturgeon.

Homeostasis of the skin barrier is essential for maintaining normal skin function. Gasdermin A (GSDMA) is highly expressed in the skin and associated with many skin diseases, such as melanoma and psoriasis. In mice, GSDMA is encoded by three gene homologues, namely Gsdma1, Gsdma2, and Gsdma3. Although Gsdma3 gain-of-function mutations cause hair loss and skin inflammation, Gsdma3-deficient mice do not show any visible phenotypes in skin and hair structures. To explore the physiological function of GSDMA, we generated conventional Gsdma1/2/3 knockout (KO) mice. These mice showed significantly alleviated epidermal hyperplasia and inflammation induced by phorbol 12-myristate 13-acetate (PMA). Furthermore, the alleviation of epidermal hyperplasia depended on the expression of Gsdma1/2/3 specifically in keratinocytes. Mechanistically, Gsdma1/2/3 depletion downregulated epidermal growth factor receptor (EGFR) ligands, leading to the decreased EGFR-Stat3/Akt signalling. These results demonstrate that depletion of Gsdma1/2/3 alleviates PMA-induced epidermal hyperplasia partially by inhibiting the EGFR-Stat3/Akt pathway., (© The Author(s) (2023). Published by Oxford University Press on behalf of Journal of Molecular Cell Biology, CEMCS, CAS.)

Perspiration and environmental chemicals, such as air pollutants, are two of the complicating factors of skin disease. It has not been studied how perspiration affect the skin responding to air pollutants. We applied topically artificial eccrine perspiration, sulphite or both to the mouse skin for one and two weeks to examine the influence of both factors on the shielding ability of healthy skin. Morphological examination showed apparent thickening of the epidermal layer in the skin samples with combined treatment at 1 week, and in the sections applied with sulphite and combined treatment at 2 weeks without significant difference in the extent of epidermal hyperplasia between two groups. The outcomes of immunohistochemical (IHC) analysis showed elevated percentages of dermal fibroblasts expressing interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), tumor necrosis factor β (TNF-β) and cyclooxygenase-2 (Cox-2). Results of two-way repeated measured analysis of variance (two-way RMANOVA) showed that both perspiration and sulphite, but not the interaction between them, were significant factors affecting the expression of proinflammatory cytokines. The evidences indicated that perspiration induced cytokines expressions in the dermal fibroblasts and promoted the effect of sulphite on the shielding response of the skin by inducing epidermis hyperplasia.

Psoriasis is a chronic immune-mediated skin disease, whose hallmarks include keratinocyte hyperproliferation and CD4+ T cell subsets imbalance. Dysregulated microRNAs (miRNAs) identified in psoriasis have been shown to affect keratinocyte and T cell functions, with studies on the molecular mechanisms and intrinsic relationships of the miRNAs on the way. Here, we focus on the dysregulated miRNAs that contribute to the two hallmarks of psoriasis with the miRNA target genes confirmed. We review a network, in which, upregulated miR-31/miR-203/miR-155/miR-21 and downregulated miR-99a/miR-125b facilitate the excessive proliferation and abnormal differentiation of psoriatic keratinocytes; upregulated miR-210 and downregulated miR-138 work in concert to distort CD4+ T cell subsets balance in psoriasis. The miRNAs exert their functions through regulating key psoriasis-associated transcription factors including NF-κB and STAT3. Whether flowing up or down, these miRNAs collaborate to promote the development and maintenance of psoriasis.

Given the increasing levels of air pollution, understanding the direct shielding response of the skin to air pollutants as a whole under exclusion of the influence from the inside of body is important. We applied topically the water soluble ambient air pollutants to the mouse skin and observed the histological response using 0.3 mM of H2SO3 as a positive control. Water soluble air pollutants samples, WSAP24h and WSA72h, were collected by pumping the outdoor air into ddH2O for 24 and 72 h respectively during two periods with different air quality index (AQI). Morphological examination showed apparent thickening of the epidermal layer in the H2SO3 skin section and in the sections applied with WSAP24h and WSAP72h without significant difference in the extent of epidermal hyperplasia among three groups. The cell viability assay showed no cytotoxic effect by the treatment of H2SO3 and WSAP24h in human skin fibroblast WS-1 cells. WSAP72h sample revealed a dose-dependent cytotoxicity to skin fibroblasts at 48 hr. The evidences indicated that the barrier function of the skin by epidermis hyperplasia could be activated by the insult of a component of air pollution, and the protection could be hold against a more complex and concentrated ambient air pollutants. [ABSTRACT FROM AUTHOR]

Background: Ultraviolet (UV) irradiation to skin induces biological responses to protect and heal the wounded tissue. Cutaneous blood vessels play an important role in maintaining skin homeostasis, by inducing angiogenesis and vasodilation. However, the vascular dynamics in vivo, such as morphological changes over time and their depth dependency, are not fully understood. Methods: Ten Asian males were enrolled in this study and received UV (UVA + UVB) irradiation at two minimal erythema dose (MED) to the inner upper arm. Changes in epidermal thickness and vascular structures associated with UV irradiation were evaluated over time for 28 days by optical coherence tomography angiography (OCTA). This technique enables non‐invasive visualization of three‐dimensional vascular networks in human skin based on OCT assessment of skin structures with near‐infrared light. Results: Notable dilation of vascular structures and increases in epidermal thickness were observed after UV irradiation. Vessel density was markedly increased from the papillary dermis to the upper reticular dermis at a depth of 200 µm. These increases in vascular density showed significant persistence even at 28 days after UV irradiation. Conclusion: We visualized the vascular structural changes caused by UV irradiation and revealed that the effects of a single UV irradiation at 2 MED persisted for up to 28 days after exposure. The OCTA technique allows not only the in situ assessment of micro‐vasculature in human skin but also its monitoring of vascular dynamics over time. [ABSTRACT FROM AUTHOR]

Photosensitivity disorder caused by sunlight, including ultraviolet (UV) rays, often occurs in connective tissue diseases such as lupus erythematosus. In addition, UVA (320-400 nM) and UVB (280-320 nM) trigger the progression of skin inflammation in the patients. Therefore, it is crucial to evaluate skin damage under UV exposure using experimental animals to clarify the relationship between connective tissue disease and photosensitivity disorder. In this chapter, our original protocol for evaluating UVA-dependent skin damage, which is known as photoaging via oxidative stress, is described., (© 2024. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

Psoriasis is a common chronic skin disease characterized by epidermal hyperplasia and inflammation. However, the pathogenesis of psoriasis is multifactorial and is not fully understood. MicroRNAs (miRNAs) represent a promising class of small, noncoding RNA molecules that have a large impact on cellular functions by regulating gene expression. Here we reported that microRNA‐187 (miR‐187), which is one of the most dynamic microRNAs identified in the deep screening miRNAs profile, is downregulated in inflammatory cytokines‐stimulated keratinocytes and psoriatic skins. By luciferase activity assay and gain‐of‐function studies, we showed that miR‐187 inhibits keratinocytes hyperproliferation by targeting CD276. Moreover, overexpression of miR‐187 decreases acanthosis and reduces the disease severity in psoriasis mouse models. Taken together, the results of our study implies miR‐187 as a critical factor in psoriasis pathogenesis, which could be a potent target for psoriasis treatment. MicroRNA‐187, which is declined in the inflammatory cytokines‐stimulated keratinocytes and psoriatic skins, can contribute to keratinocytes hyperproliferation by promoting CD276‐STAT3 signaling. [ABSTRACT FROM AUTHOR]

Fifty-six mice were classified into four groups; Group A (control group, n=8), Group B (exposure group, n=16), Group C (n=16) treated with sunscreen 15 minutes before UVB irradiations and group D (n=16) sunscreen treated 60 minutes before UVB exposure. Mice were irradiated 30 minutes 5days/week (12 weeks), and group C-D treated five days/week (12 weeks). Skin samples were taken in the mid and end of the experiment. The result of this study revealed that, epidermal thickness in group A was 7.155µm. At the mid-period of the experiment, severe epidermal hyperplasia was observed in group B with epidermal thickness 118.712µm, while in group C and D mild to moderate epidermal hyperplasia were noted with decreasing epidermal thickness to 64.154 and 90.042µm respectively. At the end of the experiment in Group B epidermal thickness reached to 281.35µm with seborrheic keratosis development, whereas in group C and D totally inhibited the development of seborrheic keratosis and epidermal thickness decreased again into 42.347 and 55.915µm. In conclusion, chronic UVB radiation-led to epidermal hyperplasia and seborrheic keratosis, sunscreen prevented the development of seborrheic keratosis and decreased the UVB-induced epidermal hyperplasia.

Ticks are blood-feeding arthropods that can transmit pathogens to humans and animals, leading to serious infectious diseases such as Lyme disease. After single or multiple tick infestation, some animal species develop resistance to tick feeding, leading to reduced risk of pathogen transmission. In mice infested with larval Haemaphysalis longicornis ticks, both mast cells and basophils reportedly play key roles in the manifestation of acquired tick resistance (ATR), but it remains ill-defined how they contribute to it. Here, we investigated their products responsible for ATR. Treatment of mice with antihistamine abolished the ATR while histamine or histamine H1 receptor agonist reduced tick-feeding even in the first infestation. In accordance with these, mice deficient for histamine production showed little or no ATR, indicating the crucial role for histamine in the expression of ATR. Adoptive transfer of mast cells and basophils derived from histamine-sufficient or deficient mice to recipient mice lacking mast cells and basophils, respectively, revealed that histamine produced by basophils but not mast cells is essential for the manifestation of ATR, in contrast to the case of local and systemic anaphylaxis where mast cell-derived histamine is the major player. During the second but not first tick infestation, basophils accumulated and made a cluster, surrounding a tick mouthpart, in the epidermis whereas mast cells were scattered and localized mainly in the dermis, more distantly from a tick mouthpart. This appears to explain why basophil-derived histamine is much more effective than mast cell-derived one. Histamine-sufficient, but not -deficient mice showed the thickened epidermis at the second tick-feeding site. Taken together, histamine released from skin-infiltrating basophils rather than skin-resident mast cells plays a crucial role in the manifestation of ATR, perhaps through promotion of epidermal hyperplasia that may inhibit tick feeding.

Background and Objective: Atopic dermatitis (AD) is a chronic inflammatory itchy skin condition. Genomic- and epigenetic wide association studies provide insights into the genetic susceptibility and potential underlying disease pathogenesis. This study sought to functionally characterise an AD-associated single nucleotide polymorphism (SNP) located deep intronic of the tight junction protein 2 (TJP2) gene (9q21.11 locus), identified through a genome-wide association study (GWAS)., Methods: The association between the 9q21.11 locus (rs7872806) and AD was identified through a GWAS of 956 cases and 723 controls. TJP2 expression in peripheral blood mononuclear cells (PBMCs) was assessed against the rs7872806 genotypes. Allele-specific methylation was evaluated at CpG sites 10kb up- and down-stream of the 9q21.11 locus. Effects of DNA methylation on TJP2 expression was validated via in vitro methylation and 5-aza-2'-deoxycytidine-induced transcriptional activation studies. Trans-epidermal water loss measurements were used to determine skin barrier function., Results: The major allele of rs7872806 was determined to increase AD risk by 2.64-fold (adjusted p-value=2.40 x 10-18, OR=0.38), associated with increased methylation levels at cg13920460 site (p<0.001) and lower TJP2 expression in PBMCs (Pearson's p=1.09 x 10-6, Pearson's R=-0.313, p<0.001). Methylation inhibition by 5-aza-2'-deoxycytidine increased TJP2 promoter activity by up to 85%. Elimination of the cg13920460 methylation site increased expression by approximately 25%. The rs7872806 major allele was also found to be associated with increased trans-epidermal water loss (p<0.001)., Conclusion: Epigenetic influence at CpG site cg13920460 is associated with rs7872806 located deep intronic at 9q21.11. The SNP confers susceptibility to AD through altering TJP2 expression and promoting trans-epidermal water loss.

Ticks are blood-feeding arthropods that can transmit pathogens to humans and animals, leading to serious infectious diseases such as Lyme disease. After single or multiple tick infestation, some animal species develop resistance to tick feeding, leading to reduced risk of pathogen transmission. In mice infested with larval Haemaphysalis longicornis ticks, both mast cells and basophils reportedly play key roles in the manifestation of acquired tick resistance (ATR), but it remains ill-defined how they contribute to it. Here, we investigated their products responsible for ATR. Treatment of mice with antihistamine abolished the ATR while histamine or histamine H1 receptor agonist reduced tick-feeding even in the first infestation. In accordance with these, mice deficient for histamine production showed little or no ATR, indicating the crucial role for histamine in the expression of ATR. Adoptive transfer of mast cells and basophils derived from histamine-sufficient or deficient mice to recipient mice lacking mast cells and basophils, respectively, revealed that histamine produced by basophils but not mast cells is essential for the manifestation of ATR, in contrast to the case of local and systemic anaphylaxis where mast cell-derived histamine is the major player. During the second but not first tick infestation, basophils accumulated and made a cluster, surrounding a tick mouthpart, in the epidermis whereas mast cells were scattered and localized mainly in the dermis, more distantly from a tick mouthpart. This appears to explain why basophil-derived histamine is much more effective than mast cell-derived one. Histamine-sufficient, but not -deficient mice showed the thickened epidermis at the second tick-feeding site. Taken together, histamine released from skin-infiltrating basophils rather than skin-resident mast cells plays a crucial role in the manifestation of ATR, perhaps through promotion of epidermal hyperplasia that may inhibit tick feeding. [ABSTRACT FROM AUTHOR]

The discovery of new therapeutic drugs with the efficacious and safe ability to prevent epidermal hyperplasia is extremely urgent for psoriasis. Cryptotanshinone (CTS), an active component isolated from the root of Salvia miltiorrhiza Bunge, has been reported to have antibacterial and antitumor effects. However, its effects on psoriasis have not been reported. Here, we investigated the therapeutic effects of CTS on imiquimod (IMQ)-induced psoriatic-like skin model and explored the underlying mechanisms. Our results revealed that CTS effectively alleviates IMQ- induced epidermal hyperplasia. In vitro studies also indicated that CTS potently inhibits the growth of keratinocytes. We further found that STAT3, a transcription factor for the cell growth, is the key mediator of CTS on the proliferation of keratinocytes. Taken together, our findings indicated that the curative effects of CTS on psoriasis are accomplished mainly through modulating STAT3, which providing evidences to develop CTS as a potential therapeutic agent for patients with psoriasis. [ABSTRACT FROM AUTHOR]

Chronic inflammatory skin diseases such as psoriasis have a significant impact on society. Currently, the major topical treatments have many side effects, making their continued use in patients difficult. Microalgae have emerged as a source of bio-active molecules such as glycolipids with potent anti-inflammatory properties. We aimed to investigate the effects of a glycolipid (MGMG-A) and a glycolipid fraction (MGDG) obtained from the microalga Isochrysis galbana on a TPA-induced epidermal hyperplasia murine model. In a first set of experiments, we examined the preventive effects of MGMG-A and MGDG dissolved in acetone on TPA-induced hyperplasia model in mice. In a second step, we performed an in vivo permeability study by using rhodamine-containing cream, ointment, or gel to determinate the formulation that preserves the skin architecture and reaches deeper. The selected formulation was assayed to ensure the stability and enhanced permeation properties of the samples in an ex vivo experiment. Finally, MGDG-containing cream was assessed in the hyperplasia murine model. The results showed that pre-treatment with acetone-dissolved glycolipids reduced skin edema, epidermal thickness, and pro-inflammatory cytokine production (TNF-α, IL-1β, IL-6, IL-17) in epidermal tissue. The in vivo and ex vivo permeation studies showed that the cream formulation had the best permeability profile. In the same way, MGDG-cream formulation showed better permeation than acetone-dissolved preparation. MGDG-cream application attenuated TPA-induced skin edema, improved histopathological features, and showed a reduction of the inflammatory cell infiltrate. In addition, this formulation inhibited epidermal expression of COX-2 in a similar way to dexamethasone. Our results suggest that an MGDG-containing cream could be an emerging therapeutic strategy for the treatment of inflammatory skin pathologies such as psoriasis. [ABSTRACT FROM AUTHOR]

The article describes a series of 12 cases of chronic hyperplastic candidiasis (CHC) with verrucous epidermal hyperplasia ( VEH), pseudocarcinomatous hyperplasia (PCH) and/or verrucous clinical appearance from the orolabial mucosa, termed verrucous candidiasis (VC). Topics covered include the histopathologic features of all cases, the clinicopathologic characteristics of VC, and the response of patients to antifungal therapy.

Background Follicular hyperkeratosis along with hyperplasia of the follicular and interfollicular epithelia are major histopathological characteristics of hidradenitis suppurativa (HS). The presence of an occasional thickening of lesional skin in some folliculitis decalvans (FD) patients and histological similarities between FD and HS led us to look for epidermal hyperplasia and follicular hyperkeratosis in FD patients. Patients and Method We performed a retrospective histological analysis of 26 patients with FD. Objective We sought to find out whether the presence of hyperplasia of the interfollicular epidermis and of the follicular epithelia could be verified in FD, with reference to the work of von Laffert et al. concerning HS. Results The main quantitative and qualitative data were: follicular hyperkeratosis (77%), hyperplasia of the interfollicular epidermis (92%) with a psoriasiform aspect (88%), atrophy of the follicular epithelia (85%), plasma cells in infiltrate (92%) in large quantities (42%), follicular microcysts (60%), atrophy of the sebaceous glands (85%) and polytrichia (54%). Conclusion Epidermal hyperplasia, sometimes psoriasiform and follicular microcysts, are significant histological signs of FD, which have been ignored until now although they seem very common. [ABSTRACT FROM AUTHOR]

Background: The pathogenesis of psoriasis is still to be fully unraveled. The immunological theory with T cells at the centre of attraction and peripherally acting cytokines are the present favourites among aetiopathological factors. Histopathology of the skin lesions offers a good study model to understand the pathogenesis of this complex disease. Aims: To study the various histopathological parameters of psoriatic lesions, and to establish their correlation with the pathogenesis of the disorder. Materials and Methods: Eighty eight consecutive histopathologically proven cases of psoriasis were included in the study. Eight common histopathological parameters of psoriasis present in these biopsies were assessed and graded. We then statistically analyzed the relationship of the factors with one another and attempted to establish a better understanding of the pathogenesis of disease. Results: Significant correlations were found between degree of epidermal hyperplasia and inflammatory infiltrate, grade of inflammation and pustules of Kogoj, inflammatory infiltrate and grade of capillary proliferation as also between epidermal hyperplasia and the presence of parakeratosis. Conclusion: The study suggests that the immunopathogenesis of psoriasis is predominantly based on the inflammatory response. This is in consonance with other studies which have suggested that psoriasis is primarily a T lymphocyte based disease. Several treatment modalities are now based on this concept and it is hoped that the future treatment modalities will focus on the central role of inflammatory cells in the pathogenesis of this enigmatic disease.

Microalgae represent a source of bio-active compounds such as carotenoids with potent anti-inflammatory and antioxidant properties. We aimed to investigate the effects of fucoxanthin (FX) in both in vitro and in vivo skin models. Firstly, its anti-inflammatory activity was evaluated in LPS-stimulated THP-1 macrophages and TNF-α-stimulated HaCaT keratinocytes, and its antioxidant activity in UVB-irradiated HaCaT cells. Next, in vitro and ex vivo permeation studies were developed to determine the most suitable formulation for in vivo FX topical application. Then, we evaluated the effects of a FX-containing cream on TPA-induced epidermal hyperplasia in mice, as well as on UVB-induced acute erythema in hairless mice. Our results confirmed the in vitro reduction of TNF-α, IL-6, ROS and LDH production. Since the permeation results showed that cream was the most favourable vehicle, FX-cream was elaborated. This formulation effectively ameliorated TPA-induced hyperplasia, by reducing skin edema, epidermal thickness, MPO activity and COX-2 expression. Moreover, FX-cream reduced UVB-induced erythema through down-regulation of COX-2 and iNOS as well as up-regulation of HO-1 protein via Nrf-2 pathway. In conclusion, FX, administered in a topical formulation, could be a novel natural adjuvant for preventing exacerbations associated with skin inflammatory pathologies as well as protecting skin against UV radiation.

Fifty-six mice were classified into four groups; Group A (control group, n=8), Group B (exposure group, n=16), Group C (n=16) treated with sunscreen 15 minutes before UVB irradiations and group D (n=16) sunscreen treated 60 minutes before UVB exposure. Mice were irradiated 30 minutes 5days/week (12 weeks), and group C-D treated five days/week (12 weeks). Skin samples were taken in the mid and end of the experiment. The result of this study revealed that, epidermal thickness in group A was 7.155µm. At the mid-period of the experiment, severe epidermal hyperplasia was observed in group B with epidermal thickness 118.712µm, while in group C and D mild to moderate epidermal hyperplasia were noted with decreasing epidermal thickness to 64.154 and 90.042µm respectively. At the end of the experiment in Group B epidermal thickness reached to 281.35µm with seborrheic keratosis development, whereas in group C and D totally inhibited the development of seborrheic keratosis and epidermal thickness decreased again into 42.347 and 55.915µm. In conclusion, chronic UVB radiation-led to epidermal hyperplasia and seborrheic keratosis, sunscreen prevented the development of seborrheic keratosis and decreased the UVB-induced epidermal hyperplasia. [ABSTRACT FROM AUTHOR]

Objective: A coccygeal pad is a nodular lesion in the sacrococcygeal area. It is a rare disease characterized by corneal thickening, the proliferation of collagen bundles, and an anterior flexed coccyx. In the English literature, 42 patients have been reported. Methods: We present a young male case of a typical coccygeal pad with an anterior flexed coccyx. Results: After resection of the nodule and coccygectomy, there has been no recurrence during the 6-month postoperative follow-up. Conclusions: Plastic surgeons should recognize this as a disease to be differentiated from gluteal skin tumors. [ABSTRACT FROM AUTHOR]