Does moisturizing the skin equate with barrier repair therapy?

Elias, Peter M.; Sugarman, Jeffrey

doi:10.1016/j.anai.2018.07.008

Cited by 20 publications

(23 citation statements)

References 43 publications

(53 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The reason for lack of uniform success after application of skin emollients requires further study, but it is important to note that not all emollients have the same effect on the skin and it has been proposed that a skin emollient that reflects the lipid composition of the skin is needed to obtain maximum benefits. 126 Other factors should also be considered, including time of introduction and adherence to therapy.…”

Section: Preventionmentioning

confidence: 99%

Cutaneous barrier dysfunction in allergic diseases

Leung

Berdyshev

Goleva

2020

Journal of Allergy and Clinical Immunology

117

112

View full text Add to dashboard Cite

The fundamental defect(s) that drives atopic dermatitis (AD) remains controversial. ''Outside in'' proponents point to the important association of filaggrin gene mutations and other skin barrier defects with AD. The ''inside out'' proponents derive support from evidence that AD occurs in genetic animal models with overexpression of type 2 immune pathways in their skin, and humans with gain-of-function mutations in their type 2 response develop severe AD. The observation that therapeutic biologics, targeting type 2 immune responses, can reverse AD provides compelling support for the importance of ''inside out'' mechanisms of AD. In this review, we propose a central role for epithelial cell dysfunction that accounts for the dual role of skin barrier defects and immune pathway activation in AD. The complexity of AD has its roots in the dysfunction of the epithelial barrier that allows the penetration of allergens, irritants, and microbes into a cutaneous milieu that facilitates the induction of type 2 immune responses. The AD phenotypes and endotypes that result in chronic skin inflammation and barrier dysfunction are modified by genes, innate/adaptive immune responses, and different environmental factors that cause skin barrier dysfunction. There is also compelling evidence that skin barrier dysfunction can alter the course of childhood asthma, food allergy, and allergic rhinosinusitis. Effective management of AD requires a multipronged approach, not only restoring cutaneous barrier function, microbial flora, and immune homeostasis but also enhancing INFORMATION FOR CATEGORY 1 CME CREDIT Credit can now be obtained, free for a limited time, by reading the review articles in this issue. Please note the following instructions.

show abstract

Section: Preventionmentioning

confidence: 99%

Cutaneous barrier dysfunction in allergic diseases

Leung

Berdyshev

Goleva

2020

Journal of Allergy and Clinical Immunology

117

112

View full text Add to dashboard Cite

show abstract

“…Maintaining normal vitamin D levels is therefore essential for development of the skin barrier (209). Moisturizers, occlusive agents, and humectants are used in AD to soften skin, create a physical barrier, and retain water (210). Experimental FLG replacement therapies currently under investigation include read-through drugs that lead to skipping of nonsense FLG mutations, drugs that regulate FLG production, FLG monomers, and FLG metabolites (12).…”

Section: Strategies To Improve the Epithelial Barrier And Prevent Allmentioning

confidence: 99%

Epithelial barrier repair and prevention of allergy

Goleva¹,

Berdyshev

Leung

2019

Journal of Clinical Investigation

165

173

View full text Add to dashboard Cite

Allergic diseases such as atopic dermatitis (AD), food allergy (FA), asthma, and allergic rhinitis affect more than 30% of the population (1-3). These diseases have in common a dysfunctional epithelial barrier, resulting in the penetration of allergens and microbes, accompanied by the release of epithelial-derived cytokines (e.g., thymic stromal lymphopoietin [TSLP], IL-25, IL-33), which drive type 2 immune responses. Although other immune pathways can modify the course of illness, cytokines including IL-4, IL-13, IL-31, TSLP, and IL-33 play a key role in allergic diseases (4-8), eliciting local tissue injury and repair (5,(9)(10)(11)(12)(13)(14).AD is the most prevalent chronic inflammatory skin disease (3,(15)(16)(17)(18)(19). In a subset of allergic patients, it is thought that ADrelated skin epithelial dysfunction contributes to the atopic march, which starts with AD and often leads directly to FA (20-23). The link from AD to respiratory allergy is more controversial; however, atopic march progression is facilitated in patients who develop IgE to both food and inhalant allergens (24).In this Review, we describe formation of the skin barrier, review the link between altered skin barrier formation and AD, discuss evidence for epithelial barrier dysfunction in other allergic diseases, and explore epithelial barrier intervention/repair strategies with the goal of preventing AD and the atopic march. The cornified envelope and keratinocyte differentiation in the skinThe skin's barrier function primarily depends on the outermost epidermal layer, stratum corneum (SC). To form SC, keratinocytes pass through a tightly regulated differentiation program and sequentially form stratum basale (SB), stratum spinosum (SS), stratum granulosum (SG), and SC layers of the skin (Figure 1). In human skin, keratinocytes irreversibly exit the cell cycle after mitosis in the basal layer and differentiate progressively across the epidermis toward the SC. Each layer is defined by its expression of characteristic morphological and biochemical features indicating its state of differentiation (25-27). The keratins KRT5 and KRT14 are predominantly expressed by basal keratinocytes. The markers of early differentiation KRT1 and KRT10 are made in SS. The cornified envelope precursors involucrin (IVL) and transglutaminase-1 (TGM1) are also present in SS. Late differentiation markers including the cornified envelope protein loricrin (LOR) and the precursor of the keratin cross-linking protein filaggrin (FLG) are expressed in SG keratinocytes. TGM1 cross-links IVL, LOR, and other structural proteins to form the cornified envelope.Calcium forms a steep gradient across the human epidermis, increasing from the SB (5 μM) to the outer SG (>20 μM) (27, 28). Importantly, there is cell-to-cell heterogeneity in average Ca 2+ concentrations in the epidermis (28). Formation of the Ca 2+ gradient coincides with key developmental milestones of skin barrier formation and differentiation into the SC.Primary human keratinocyte cultures are an excellent model for...

show abstract

“…There are many types of moisturizers, and not all are designed to or capable of mitigating xerosis . While occlusive agents coat the skin with friction‐reducing substances like silicones to increase skin smoothness, their benefits are temporary . More than just coating the surface of skin, effective moisturizers are capable of improving skin barrier homeostasis and function.…”

Section: Discussionmentioning

confidence: 99%

“…All three barrier lipids are needed for proper maturation and natural skin desquamation in the stratum corneum . Notably, atopic dermatitis is characterized by a reduction in all three key barrier lipids . Corneocytes, where filaggrin originates, are embedded in the barrier lipids of the stratum corneum and have a primary role in supporting barrier function .…”

Section: Introductionmentioning

confidence: 99%

In vitro and in vivo evaluation of a moisture treatment cream containing three critical elements of natural skin moisturization

Dover

Wortzman²,

Nelson³

2020

J of Cosmetic Dermatology

View full text Add to dashboard Cite

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractObjectives: To evaluate skin barrier and hydration effects of a new rebalancing moisture treatment (TRMT) and to assess efficacy and tolerability in subjects with photodamaged skin. Methods:In an epidermal skin model, tissues (n = 5/group) were topically treated with 25 µL of TRMT, 25 µL of a market-leading moisturizer (MLM), or untreated for 60 minutes. Hydration was measured at 0, 15, and 30 minutes. Tissues were harvested for gene expression analysis of markers associated with skin barrier and hydration: Claudin (CLD), Aquaporin (AQP), Hyaluronic Acid Syntheses (HAS), and Hyaluronidase (HYAL). A clinical study evaluated twice-daily application of TRMT, assessing changes in fine lines/wrinkles, brightness, texture, erythema, and tolerability from baseline through week 8. Hydration was measured using electrical impedance.Results: TRMT and MLM demonstrated significant increases in hydration vs untreated tissue at each timepoint (P < .005), with greater hydration effects observed for TRMT vs MLM. TRMT-treated tissues demonstrated greater expression of CLD, AQP, and HA, and reduced expression of HYAL vs untreated and MLM-treated tissues. Twice-daily application of TRMT demonstrated significant improvements at 2 weeks in fine lines/wrinkles (P < .001), brightness (P < .0001), texture (P < .0004), and hydration (P < .004). At 8 weeks, statistically significant improvements were achieved in all categories. Conclusion:In an epidermal skin model, TRMT demonstrated significant increases in hydration, greater hydration effects, and expression of key markers associated with skin barrier and hydration vs a MLM. Twice-daily application of TRMT was well tolerated and resulted in early, significant improvements in hydration and visible improvements in skin brightness, texture, fine lines/wrinkles, and erythema at 8 weeks. K E Y W O R D Scosmeceutical, hydration, moisturizing, photoaging of the skin, skin barrier

show abstract

Does moisturizing the skin equate with barrier repair therapy?

Cited by 20 publications

References 43 publications

Cutaneous barrier dysfunction in allergic diseases

Cutaneous barrier dysfunction in allergic diseases

Epithelial barrier repair and prevention of allergy

In vitro and in vivo evaluation of a moisture treatment cream containing three critical elements of natural skin moisturization

Contact Info

Product

Resources

About