Epidermal Barriers Research Articles

The water extracts from the oil cakes of Prinsepia utilis repair the epidermal barrier via up-regulating Corneocyte Envelope-proteins, lipid synthases, and tight junction proteins

Ethnopharmacological relevancePrinsepia utilis Royle, native to the Himalayan region, has a long history of use in traditional medicine for its heat-clearing, detoxification, anti-inflammatory, and analgesic properties. Oils extracted from P. utilis seeds are also used in cooking and cosmetics. With the increasing market demand, this extraction process generates substantial industrial biowastes. Recent studies have found many health benefits with using aqueous extracts of these biowastes, which are also rich in polysaccharides. However, there is limited research related to the reparative effects of the water extracts of P. utilis oil cakes (WEPUOC) on disruptions of the skin barrier function. Aim of the studyThis study aimed to evaluate the reparative efficacy of WEPUOC in both acute and chronic epidermal permeability barrier disruptions. Furthermore, the study sought to explore the underlying mechanisms involved in repairing the epidermal permeability barrier. Materials and methodsMouse models with induced epidermal disruptions, employing tape-stripping (TS) and acetone wiping (AC) methods, were used. The subsequent application of WEPUOC (100 mg/mL) was evaluated through various assessments, with a focus on the upregulation of mRNA and protein expression of Corneocyte Envelope (CE) related proteins, lipid synthase-associated proteins, and tight junction proteins. ResultsThe polysaccharide was the major phytochemicals of WEPUOC and its content was determined as 32.2% by the anthranone-sulfuric acid colorimetric method. WEPUOC significantly reduced transepidermal water loss (TEWL) and improved the damaged epidermal barrier in the model group. Mechanistically, these effects were associated with heightened expression levels of key proteins such as FLG (filaggrin), INV (involucrin), LOR (loricrin), SPT, FASN, HMGCR, Claudins-1, Claudins-5, and ZO-1. ConclusionsWEPUOC, obtained from the oil cakes of P. utilis, is rich in polysaccharides and exhibits pronounced efficacy in repairing disrupted epidermal barriers through increased expression of critical proteins involved in barrier integrity. Our findings underscore the potential of P. utilis wastes in developing natural cosmetic prototypes for the treatment of diseases characterized by damaged skin barriers, including atopic dermatitis and psoriasis.

Semaglutide (Ozempic) and obesity. A comprehensive guide for aestheticians

Obesity is a complex interplay of biological, genetic, behavioural, and environmental factors. Going beyond the con- ventional Body Mass Index (BMI) evaluation, the complex relationship between obesity and skin diseases unveils the evolving role of aesthetics in health promotion. Adipose tissue, traditionally seen as an energy reservoir, is unveiled as a dynamic endocrine organ, playing a crucial role in the pathophysiological mechanisms of insulin resistance and metabolic syndrome. This article navigates the skin-deep impact of obesity and unravelling its influence on dermato- logical challenges. From disrupted epidermal barriers to diseases such as psoriasis and hidradenitis suppurativa, it further explores how licensed cosmetologists emerge as health advocates. For what is more, semaglutide, a ground- breaking GLP-1 agonist, takes the spotlight, tracing its journey from FDA approval for type 2 diabetes to its recent endorsement for obesity. The article examines its mechanism, efficacy, and unintended consequences of popularity, emphasizing the need for responsible medication use.

Oat β-glucan repairs the epidermal barrier by upregulating the levels of epidermal differentiation, cell-cell junctions and lipids via Dectin-1.

Oat β-glucan could ameliorate epidermal hyperplasia and accelerate epidermal barrier repair. Dectin-1 is one of the receptors of β-glucan and many biological functions of β-glucan are mediated by Dectin-1. Dectin-1 promotes wound healing through regulating the proliferation and migration of skin cells. Thus, this study aimed to investigate the role of oat β-glucan and Dectin-1 in epidermal barrier repair. To investigate the role of Dectin-1 in the epidermal barrier, indicators associated with the recovery of a damaged epidermal barrier, including histopathological changes, keratinization, proliferation, apoptosis, differentiation, cell-cell junctions and lipid content were compared between WT and Dectin-1-/- mice. Further, the effect of oat β-glucan on the disruption of the epidermal barrier was also compared between WT and Dectin-1-/- mice. Dectin-1 deficiency resulted in delayed recovery and marked keratinization, as well as abnormal levels of keratinocyte differentiation, cell-cell junctions and lipid synthesis during the restoration of the epidermal barrier. Oat β-glucan significantly reduces epidermal hyperplasia, promotes epidermal differentiation, increases cell-cell junction expression, promotes lipid synthesis and ultimately accelerates the recovery of damaged epidermal barriers via Dectin-1. Oat β-glucan could promote CaS receptor expression and activate the PPAR-γ signalling pathway via Dectin-1. Oat β-glucan promote the recovery of damaged epidermal barriers through promoting epidermal differentiation, increasing the expression of cell-cell junctions and lipid synthesis through Dectin-1. Dectin-1 deficiency delay the recovery of epidermal barriers, which indicated that Dectin-1 may be a potential target in epidermal barrier repair.

Comparative immunohistochemical analysis suggests a conserved role of EPS8L1 in epidermal and hair follicle barriers of mammals.

The mammalian skin and its appendages depend on tightly coordinated differentiation of epithelial cells. Epidermal growth factor receptor (EGFR) pathway substrate 8 (EPS8) like 1 (EPS8L1) is enriched in the epidermis among human tissues and has also been detected in the epidermis of lizards. Here, we show by the analysis of single-cell RNA-sequencing data that EPS8L1 mRNA is co-expressed with filaggrin and loricrin in terminally differentiated human epidermal keratinocytes. Comparative genomics indicated that EPS8L1 is conserved in all main clades of mammals, whereas the orthologous gene has been lost in birds. Using a polyclonal antibody against EPS8L1, we performed an immunohistochemical screening of skin from diverse mammalian species and immuno-electron microscopy of human skin. EPS8L1 was detected predominantly in the granular layer of the epidermis in monotremes, marsupial, and placental mammals. The labeling was partly associated with cell membranes, and it was evident along the perimeter of keratinocytes at the transition with the cornified layer of the epidermis, similar to involucrin distribution. Basal, spinous, and the fully mature cornified layers lacked immunolabeling of EPS8L1. In addition to the epidermis, the hair follicle inner root sheath (IRS) was immunolabeled. Both epidermal granular layer and IRS contribute to the barrier function of the skin, suggesting that EPS8L1 is involved in the regulation of these barriers.

Ex Vivo Infection of Human Skin Models with Herpes Simplex Virus 1: Accessibility of the Receptor Nectin-1 during Formation or Impairment of Epidermal Barriers Is Restricted by Tight Junctions.

Herpes simplex virus 1 (HSV-1) must overcome epidermal barriers to reach its receptors on keratinocytes and initiate infection in human skin. The cell-adhesion molecule nectin-1, which is expressed in human epidermis, acts as an efficient receptor for HSV-1 but is not within reach of the virus upon exposure of human skin under nonpathological conditions. Atopic dermatitis skin, however, can provide an entry portal for HSV-1 emphasizing the role of impaired barrier functions. Here, we explored how epidermal barriers impact HSV-1 invasion in human epidermis and influence the accessibility of nectin-1 for the virus. Using human epidermal equivalents, we observed a correlation of the number of infected cells with tight-junction formation, suggesting that mature tight junctions prior to formation of the stratum corneum prevent viral access to nectin-1. Consequently, impaired epidermal barriers driven by Th2-inflammatory cytokines interleukin 4 (IL-4) and IL-13 as well as the genetic predisposition of nonlesional atopic dermatitis keratinocytes correlated with enhanced infection supporting the impact of functional tight junctions for preventing infection in human epidermis. Comparable to E-cadherin, nectin-1 was distributed throughout the epidermal layers and localized just underneath the tight-junctions. While nectin-1 was evenly distributed on primary human keratinocytes in culture, the receptor was enriched at lateral surfaces of basal and suprabasal cells during differentiation. Nectin-1 showed no major redistribution in the thickened atopic dermatitis and IL-4/IL-13-treated human epidermis in which HSV-1 can invade. However, nectin-1 localization toward tight junction components changed, suggesting that defective tight-junction barriers make nectin-1 accessible for HSV-1 which enables facilitated viral penetration. IMPORTANCE Herpes simplex virus 1 (HSV-1) is a widely distributed human pathogen which productively infects epithelia. The open question is which barriers of the highly protected epithelia must the virus overcome to reach its receptor nectin-1. Here, we used human epidermal equivalents to understand how physical barrier formation and nectin-1 distribution contribute to successful viral invasion. Inflammation-induced barrier defects led to facilitated viral penetration strengthening the role of functional tight-junctions in hindering viral access to nectin-1 that is localized just underneath tight junctions and distributed throughout all layers. We also found nectin-1 ubiquitously localized in the epidermis of atopic dermatitis and IL-4/IL-13-treated human skin implying that impaired tight-junctions in combination with a defective cornified layer allow the accessibility of nectin-1 to HSV-1. Our results support that successful invasion of HSV-1 in human skin relies on defective epidermal barriers, which not only include a dysfunctional cornified layer but also depend on impaired tight junctions.

Calcitriol, an Active Form of Vitamin D3, Mitigates Skin Barrier Dysfunction in Atopic Dermatitis NC/Nga Mice.

Atopic dermatitis and psoriasis are prevalent chronic inflammatory skin diseases that are characterized by dysfunctional skin barriers and substantially impact patients' quality of life. Vitamin D3 regulates immune responses and keratinocyte differentiation and improves psoriasis symptoms; however, its effects on atopic dermatitis remain unclear. Here, we investigated the effects of calcitriol, an active form of vitamin D3, on an NC/Nga mouse model of atopic dermatitis. We observed that the topical application of calcitriol decreased the dermatitis scores and epidermal thickness of NC/Nga mice with atopic dermatitis compared to untreated mice. In addition, both stratum corneum barrier function as assessed by the measurement of transepidermal water loss and tight junction barrier function as evaluated by biotin tracer permeability assay were improved following calcitriol treatment. Moreover, calcitriol treatment reversed the decrease in the expression of skin barrier-related proteins and decreased the expression of inflammatory cytokines such as interleukin (IL)-13 and IL-33 in mice with atopic dermatitis. These findings suggest that the topical application of calcitriol might improve the symptoms of atopic dermatitis by repairing the dysfunctional epidermal and tight junction barriers. Our results suggest that calcitriol might be a viable therapeutic agent for the treatment of atopic dermatitis in addition to psoriasis.

725 Revisiting the importance of epidermal barriers to maintain epidermal and dermal conditions

725 Revisiting the importance of epidermal barriers to maintain epidermal and dermal conditions

Natural polyphenols: a promising bioactive compounds for skin care and cosmetics

The physiological and morphological aspects of skin suffer from frequent change. Numerous internal and external factors have direct impact on inducing various skin problems like inflammation, aging, cancer, oxidative stress, hyperpigmentation etc. The use of plant polyphenols as a photo-ecting agent is gaining popularity nowadays. Polyphenols are known to enhance endogenic antioxidant system of skin thereby preventing various skin diseases. The biological activity of plant polyphenols is dependent on their physicochemical properties for overcoming the epidermal barriers to reach the specific receptor. Several evidences have reported the vital role polyphenols in mitigating adverse skin problems and reverting back the healthy skin condition. The interest in plant derived skin care products is emerging due to the changing notion of people to shift their focus towards use of plant-based products. The present review draws an attention to uncover the protective role of polyphenols in prevention of various skin problems. Several in vitro and in vivo studies have been summarized that claims the efficacious nature of plant extract having dermatological significance.

Keratinocytes: An Enigmatic Factor in Atopic Dermatitis.

Atopic dermatitis (AD), characterized by rashes, itching, and pruritus, is a chronic inflammatory condition of the skin with a marked infiltration of inflammatory cells into the lesion. It usually commences in early childhood and coexists with other atopic diseases such as allergic rhinitis, bronchial asthma, allergic conjunctivitis, etc. With a prevalence rate of 1–20% in adults and children worldwide, AD is gradually becoming a major health concern. Immunological aspects have been frequently focused on in the pathogenesis of AD, including the role of the epidermal barrier and the consequent abnormal cytokine expressions. Disrupted epidermal barriers, as well as allergic triggers (food allergy), contact allergens, irritants, microbes, aggravating factors, and ultraviolet light directly initiate the inflammatory response by inducing epidermal keratinocytes, resulting in the abnormal release of various pro-inflammatory mediators, inflammatory cytokines, and chemokines from keratinocytes. In addition, abnormal proteinases, gene mutations, or single nucleotide polymorphisms (SNP) affecting the function of the epidermal barrier can also contribute towards disease pathophysiology. Apart from this, imbalances in cholinergic or adrenergic responses in the epidermis or the role played by immune cells in the epidermis such as Langerhans cells or antigen-presenting cells can also aggravate pathophysiology. The dearth of specific biomarkers for proper diagnosis and the lack of a permanent cure for AD necessitate investigation in this area. In this context, the widespread role played by keratinocytes in the pathogenesis of AD will be reviewed in this article to facilitate the opening up of new avenues of treatment for AD.

Small, Cationic Antifungal Proteins from Filamentous Fungi Inhibit Candida albicans Growth in 3D Skin Infection Models.

ABSTRACTThe emerging resistance of human-pathogenic fungi to antifungal drugs urges the development of alternative therapeutic strategies. The small, cationic antifungal proteins (AFPs) from filamentous ascomycetes represent promising candidates for next-generation antifungals. These bio-molecules need to be tested for tolerance in the host and efficacy against fungal pathogens before they can be safely applied in humans. Testing of the efficacy and possible adverse effects of new drug candidates in three-dimensional (3D) human-cell based models represents an advantageous alternative to animal experiments. In, this study, as a proof-of-principle, we demonstrate the usefulness of 3D skin infection models for screening new antifungal drug candidates for topical application. We established a cutaneous infection with the opportunistic human-pathogenic yeast Candida albicans in a commercially available 3D full-thickness (FT) skin model to test the curative potential of distinct AFPs from Penicillium chrysogenum (PAFopt, PAFB, and PAFC) and Neosartorya (Aspergillus) fischeri (NFAP2) in vitro. All tested AFPs were comparably well tolerated by the skin models. The infected 3D models exhibited reduced epidermal permeability barriers, allowing C. albicans to colonize the epidermal and dermal layers, and showed increased secretion of the pro-inflammatory cytokine IL-6 and the chemokine IL-8. AFP treatment diminished the fungal burden and penetration depth of C. albicans in the infected models. The epidermal permeability barrier was restored and the secretion of IL-8 was decreased following AFP treatment. In summary, our study proves that the tested AFPs exhibit antifungal potential against cutaneous C. albicans infection in a 3D FT skin model.IMPORTANCE Candida albicans represents one of the most prevalent opportunistic fungal pathogens, causing superficial skin and mucosal infections in humans with certain predisposing health conditions and life-threatening systemic infections in immunosuppressed patients. The emerging drug resistance of this human-pathogenic yeast and the limited number of antifungal drugs for prevention and treatment of infections urgently demands the identification of new antifungal compounds with novel mechanisms of action. Small, cationic antifungal proteins (AFPs) from filamentous fungi represent promising candidates for next-generation antifungals for topical application. These bio-molecules need to be tested for tolerance by the host and efficacy in pathogen clearance prior to being involved in clinical trials. In a proof-of-principle study, we provide evidence for the suitability of 3D human-cell based models as advantageous alternatives to animal experiments. We document the tolerance of specific AFPs and their curative efficacy against cutaneous C. albicans infection in a 3D skin model.

Immunomodulatory Role of Staphylococcus aureus in Atopic Dermatitis

Staphylococcus aureus is a gram-positive bacterium commonly found on humans, and it constitutes the skin microbiota. Presence of S. aureus in healthy individuals usually does not pose any threat, as the human body is equipped with many mechanisms to prevent pathogen invasion and infection. However, colonization of S. aureus has been correlated with many healthcare-associated infections, and has been found in people with atopic diseases. In atopic dermatitis, constant fluctuations due to inflammation of the epidermal and mucosal barriers can cause structural changes and allow foreign antigens and pathogens to bypass the first line of defense of the innate system. As they persist, S. aureus can secrete various virulence factors to enhance their survival by host invasion and evasion mechanisms. In response, epithelial cells can release damage-associated molecular patterns, or alarmins such as TSLP, IL-25, IL-33, and chemokines, to recruit innate and adaptive immune cells to cause inflammation. Until recently, IL-36 had been found to play an important role in modulating atopic dermatitis. Secretion of IL-36 from keratinocytes can activate a Th2 independent pathway to trigger symptoms of allergic reaction resulting in clinical manifestations. This mini review aims to summarize the immunomodulatory roles of S. aureus virulence factors and how they contribute to the pathogenesis of atopic diseases.

Chlorhexidine \u2013 a commonly used but often neglected culprit of dialysis associated anaphylactic reactions (case report)

BackgroundHemodialysis-associated anaphylactic reactions are rare and frequently complex in nature due to the sheer number of possible culprit agents. Unfortunately, dialysis is often unavoidable or strictly essential for life-saving solute clearance or fluid removal in patients with end stage kidney failure and those with severe acute kidney injury. It is of utmost importance that the culprit agent is identified and avoided to allow continuation of dialysis treatment as needed.Case presentationWe present 2 cases of hemodialysis-associated anaphylactic reactions. These patients developed anaphylactic reactions peri-dialysis and were initially suspected to have dialyser reactions. They were investigated in a controlled healthcare setting and possible culprit agents were systemically identified and eliminated. They both underwent allergy testing and were diagnosed with chlorhexidine allergy. Of note, Case 1 was an incident dialysis patient at the time of presentation and Case 2 was a prevalent dialysis patient. This suggests that the time from initial sensitization to reaction may not always be helpful in determining if a particular agent is the culprit of an anaphylactic reaction.In both cases, the patients were dialysed through a tunnelled dialysis catheter. We postulate that the presence of an exit site, which represents a compromise to the integrity of the skin’s epidermal barrier, may have a significant role in the development of these reactions.As chlorhexidine is a widely used disinfectant in hemodialysis, it is imperative that we consider it as a possible culprit agent when these reactions arise. To our knowledge, there are no other reported cases of anaphylaxis secondary to chlorhexidine use in dialysis patients other than a previous report in 2017.Our report also highlights the possibility of these reactions occurring more frequently in patients with damaged epidermal barriers and in patients exposed to higher environmental concentrations of chlorhexidine. These are novel concepts that can be explored with further research.ConclusionChlorhexidine associated anaphylactic reactions can occur in the peri-dialysis setting and a high index of suspicion is paramount to diagnosis.

Understanding the key issues in the treatment of uncontrolled persistent asthma with type 2 inflammation.

Asthma is a complex respiratory disease that varies in severity and response to treatment. Several asthma phenotypes with unique clinical and inflammatory characteristics have been identified. Endotypes, based on distinct molecular profiles, help to further elucidate the heterogeneity within asthma. Type 2 inflammation, involving both the innate (type 2 innate lymphoid cell) and adaptive (T-helper type 2 cells) immune systems, underpins the complex pathophysiology of chronic inflammation in asthma, as well as the presence of comorbid disease (e.g. chronic rhinosinusitis with nasal polyps, allergic rhinitis and atopic dermatitis). Type 2 inflammation is characterised by upregulation of the type 2 cytokines interleukin (IL)-4, IL-5 and IL-13, IgE-mediated release of immune mediators and dysfunction of epithelial or epidermal barriers. Targeting these key proximal type 2 cytokines has shown efficacy in recent studies adopting a personalised approach to treatment using targeted biologics. Elevated levels of biomarkers downstream of type 2 cytokines, including fractional exhaled nitric oxide, serum IgE and blood and sputum eosinophils, have been linked to mechanisms involved in type 2 inflammation. They have the potential to aid diagnosis, and to predict and monitor response to treatment. The objective of this review is to summarise the current understanding of the biology of type 2 inflammation in asthma, examine its influence on type 2 inflammatory comorbidities, and discuss how type 2 inflammatory biomarkers can be harnessed to further personalise treatments in the age of biologic medicines.

Immunopathogenesis of Dermatophytoses and Factors Leading to Recalcitrant Infections.

The pathogenesis of dermatophytic infections involves the interplay of three major factors: the dermatophyte, the inherent host defense, and the adaptive host immune response. The fungal virulence factors determine the adhesion and invasion of the skin while the immune response depends on an interaction of the pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMP) with pattern recognition receptors (PRRs) of the host, which lead to a differential Th (T helper) 1, Th2, Th17, and Treg response. While anthropophilic dermatophytes Trichophyton rubrum and now increasingly by T. interdigitale subvert the immune response via mannans, zoophilic species are eliminated due to a brisk immune response. Notably, delayed-type hypersensitivity (Th1) response of T lymphocytes causes the elimination of fungal infection, while chronic disease caused by anthropophilic species corresponds to toll-like receptor 2 mediated IL (interleukin)-10 release and generation of T-regulatory cells with immunosuppressive potential. Major steps that determine the ultimate clinical course and chronicity include genetic susceptibility factors, impaired epidermal and immunological barriers, variations in the composition of sebum and sweat, carbon dioxide tension, skin pH, and topical steroid abuse. It is important to understand these multifarious aspects to surmount the problem of recalcitrant dermatophytosis when the disorder fails conventional therapeutic agents.

Immunohistochemical study of CD117 in various cutaneous melanocytic lesions.

The aim of the present study was to carried out a comparative immunohistochemical evaluation of CD117 (c-Kit), a biomarker that evaluates both tumor progression and prognosis, in different melanocytic lesions, to emphasize the significance of this biomarker in malignant melanoma (MM). The study was performed on 55 cases, represented by a control group, which included 5 cases of simple nevi and 5 cases of dysplastic nevi, as well as a study group consisting of 35 cases of primary MM and 10 metastases (one intestinal, 3 cutaneous - one satellite and two distant as well as 6 in the lymph nodes). The study group included 15 cases of superficial spreading melanoma (SSM), 10 cases of nodular melanoma (NM), 3 lentigo maligna melanoma (LMM), 3 cases of acral lentiginous melanoma (ALM) and 4 cases of amelanotic MM. CD117 was found to be massively involved in the process of tumorigenesis of cutaneous malignancies, being immunohistochemically undetectable in benign neural lesions, but densely expressed in dysplastic lesions and in situ melanoma areas. In invasive cutaneous MMs, CD117 expression tended to decrease with neoplasia progression proceding into the tumorigenic, vertical growth phase, being lower in the profound dermal component of tumors and in nodular MMs. To eliminate the epidermal barriers and gain a proliferative advantage to allow the transition to the vertical growth phase, it seems that MM should lose expression of c-Kit. Cutaneous metastases were found to express CD117 at a level comparable to their primary tumors, suggesting that other mechanisms interfere directly with the metastatic process and not loss of c-Kit expression by itself. CD117 overexpression in cutaneous melanocytic lesions correlates significantly with increased immunostaining intensity, suggesting that the immunohistochemical evaluation of CD117 may be a good method for screening patients, who could benefit from personalized therapy with tyrosine kinase inhibitors.

Metformin loaded cholesterol-lysine conjugate nanoparticles: A novel approach for protecting HDFs against UVB-induced senescence.

Cellular senescence is one of the hallmarks of aging. Since senescence of dermal fibroblasts has been reported in vivo, reduction of the deleterious effects of these cells, has been considered an important intervention to counteract skin aging. Promising anti-aging effect of metformin has been reported. However, permeation of metformin due to its high hydrophilicity through skin epidermal barriers is limited. In this study, solid lipid nanoparticles (SLNs) of metformin were designed with the newly synthesized cholesterol-lysine conjugate as lipid for topical delivery of metformin. Characterization of SLNs strongly confirmed the effect of cholesterol-lysine conjugate on increasing entrapment of metformin. The designed SLNs with particle size of 283nm and spherical morphology represented controlled drug release up to 18days. Fluorescent tracking of SLNs on mice skin samples showed an increase in epidermal penetration. SLNs containing metformin showed anti-senescence effects on UVB-induced senescence of human dermal fibroblasts, this effect was confirmed by senescence-associated β-galactosidase staining, RT q-PCR and cell cycle analyses. Furthermore, our drug-free SLNs showed anti-senescence effects, suggesting that they can be a suitable carrier for phytochemicals with anti-aging effect or other hydrophilic compounds which have constraints permeating skin.

Comparison of transepidermal water loss rates in subjects with skin patch test positive vs negative to skin care products

Adverse cutaneous reactions to skin care products (SCP) are becoming increasingly common and may be indicative of defective permeability barrier function. To determine the differences in transepidermal water loss rates (TEWL) between skin patch positive vs negative to skin care products in normal Chinese females. Skin patch test reactions to nine skin care products were assessed in 65 normal Chinese females. Correlations of cutaneous reactions to a panel of nine foreign and domestic SCP with permeability barrier function and stratum corneum (SC) hydration levels were analyzed. Out of 65 subjects, 24 (37%) displayed positive reactions to one or more SCP. However, the occurrence of positive reactions to patch tests did not correlate with either transepidermal water loss rates or SC hydration levels. Though a substantial proportion of normal females display adverse reactions to SCP, this problem cannot be attributed to differences in the qualities of their epidermal permeability barriers, and therefore, these reactions more likely reflect the potential adverse events of the SCP themselves. However, further studies in large cohort of both males and females would be helpful to ascertain whether TEWL levels can predict cutaneous reactions to SCP.

Abalone Collagen Extracts Potentiate Stem Cell Properties of Human Epidermal Keratinocytes.

Stem cell activities in human tissues are critical for tissue integrity and function. Maintaining keratinocyte stem cells (KSCs) stemness helps sustain healthy skin by supporting keratinocyte renewal, involving the formation of epidermal barriers. In this study, abalone collagen (AC) extracts with molecular weights of 3 kDa (AC 1) and 300 kDa (AC 2) were compared to the epidermal growth factor (EGF) for their effects on cell proliferation, cell migration (wound healing), spheroid formation, and the expression level of stem cell markers on human keratinocytes (HaCaT cells). Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and cell proliferation was quantified by ATP and DNA content analysis and Sulforhodamine B (SRB) assays. Cell migration assay was determined using the scratch wound healing test. Spheroid formation was evaluated and the expression level of stem cell markers was investigated by western blot analysis. The results showed that AC 1 at the concentration of 100 µg/mL could stimulate HaCaT cell proliferation, migration, spheroid formation, and the expression level of stem cell markers (keratin 19, β-catenin, ALDH1A1) compared to the control. In conclusion, a smaller molecular weight of abalone collagen extract exhibits a better effect on keratinocytes proliferation, migration, and stemness, which could be a potential active ingredient in cosmeceutical products.

Intracellular Invasion by Streptococcus pyogenes: Invasins, Host Receptors, and Relevance to Human Disease.

The human oral-nasal mucosa is the primary reservoir for Streptococcus pyogenes infections. Although the most common infection of consequence in temperate climates is pharyngitis, the past 25 years have witnessed a dramatic increase in invasive disease in many regions of the world. Historically, S. pyogenes has been associated with sepsis and fulminate systemic infections, but the mechanism by which these streptococci traverse mucosal or epidermal barriers is not understood. The discovery that S. pyogenes can be internalized by mammalian epithelial cells at high frequencies (1-3) and/or open tight junctions to pass between cells (4) provides potential explanations for changes in epidemiology and the ability of this species to breach such barriers. In this article, the invasins and pathways that S. pyogenes uses to reach the intracellular state are reviewed, and the relationship between intracellular invasion and human disease is discussed.

Contact Dermatitis in the Patient with Atopic Dermatitis

Atopic dermatitis (AD) and allergic contact dermatitis (ACD) are common T-cell-mediated inflammatory skin conditions that can share clinical presentations. The variable expression of ACD among patients with AD represents the shades of gray of the multifaceted relationship between the 2 disorders, where increased allergen permeation in compromised epidermal barriers augments antigen presentation and sensitization, with subsequent immune dysregulation. Further studies are needed to define the relationship and immunologic intersection points of these 2 conditions.