A deficient epidermal barrier is a key feature of atopic dermatitis (AD) and comprises altered lipid and protein content and composition of the stratum corneum resulting in disturbed water balance. Clinically, eczematous lesions on dry skin and pruritus develop. Pruritic nodules occur in prurigo nodularis (PN), another chronic skin disease, which can be associated with atopy. We aimed at comparing the three clinical pictures, classic AD, atopic prurigo (AP), and non-atopic PN, to healthy controls regarding the epidermal barrier. We determined clinical parameters and performed biophysical measurements, histology/immunohistochemistry, electron microscopy, and molecular biological analysis. We found distinctively elevated clinical scores, reduced hydration and increased transepidermal water loss, epidermal hyperplasia and inflammation reduced filaggrin and increased loricrin and involucrin expression, as well as reduced intercellular lipid lamellae in all three disease groups. These findings show a severe disruption in epidermal barrier structure and function in all three disorders so that epidermal barrier impairment is now proven not only for AD but also for PN.

Steroid hormones became increasingly interesting as active pharmaceutical ingredients for the treatment of endocrine disorders. However, medical applications of many steroidal drugs are inhibited by their very low aqueous solubilities giving rise to low bioavailabilities. Therefore, the prioritized oral administration of steroidal drugs remains problematic. Cyclodextrins are promising candidates for the development of drug delivery systems for oral route applications, since they solubilize hydrophobic steroids and increase their rate of transport in aqueous environments. In this study, the synthesis and characterization of polymeric β-cyclodextrin derivates is described, which result from the attachment of a hydrophilic β-CD-thioether to hyaluronic acid. Host-guest complexes of the synthesized β-cyclodextrin hyaluronic acid conjugates were formed with two poorly soluble model steroids (β-estradiol, dexamethasone) and compared to monomeric β-cyclodextrin derivates regarding solubilization and complexation efficiency. The β-cyclodextrin-drug (host-guest) complexes were evaluated in vitro for their suitability (cytotoxicity and transport rate) as intestinal drug carriers for steroid hormones. In case of β-estradiol, higher solubilities could be achieved by complexation with both synthesized β-cyclodextrin derivates, leading to significantly higher intestinal transport rates in vitro. However, this success could not be shown for dexamethasone, which namely solubilized better, but could not enhance the transport rate significantly. Thus, this study demonstrates the biocompatibility of the synthesized and characterized β-cyclodextrin derivates and shows their potential as new candidate for intestinal drug carrier for steroid hormones like β-estradiol.

Efficient chemical modification of cellulose nanocrystals (CNCs) by grafting commonly involves aprotic solvents, toxic reactants, harsh reaction conditions, or catalysts, which have negative effects on the particle character, reduced dispersibility and requires further purification, if products are intended for biomedical applications. This work, in contrast, presents a robust, facile, and green synthesis protocol for the grafting of an amino-reactive fluorophore like fluorescein isothiocyanate (FITC) on aqueous CNCs, combining and modifying existent approaches in a two-step procedure. Comparably high grafting yields were achieved, which were confirmed by thermogravimetry, FTIR, and photometry. The dispersive properties were confirmed by DLS, AF4-MALS, and TEM studies. The presented route is highly suitable for the introduction of silane-bound organic groups and offers a versatile platform for further modification routes of cellulose-based substrates.

Introduction This pilot study investigated the effects of a 12-week administration of a nutritional supplement containing special collagen peptides on the structural and molecular properties of the collagen fiber network in the human skin. For the assessments, the suction blister method and electron microscopical comparisons were used. Methods Three suction blisters were generated on the inner forearm of each test subject before and after the 12-week administration of the nutritional supplement. High-resolution scanning electron microscopy (SEM) was employed to meticulously investigate the structural characteristics of the skin’s collagen network, including the length and diameter of collagen fibers within the suction blister roof. Furthermore, the analysis included immunohistochemistry and fluorescence light microscopy to study hyaluronic acid within the extracellular matrix. Additional assessments encompassed changes in various epidermal parameters. Nine female participants within the age range of 43.7–61.8 years (mean: 52.5 ± 5.9 years) completed the study in accordance with the study protocol. Results Compared with baseline, the 12-week supplementation regimen led to a statistically significant average increase in the collagen fiber network size of 34.56% (p < 0.0001). Additionally, collagen fiber cross-linking and fiber length were substantially increased. The ingestion of the supplement also resulted in an 18.08% elevation in epidermal hyaluronic acid concentration (p < 0.0001). No adverse events were recorded during the study. Conclusion Using an innovative approach, this study demonstrated the ability of a targeted nutritional supplement to effectively restore the ultrastructural integrity of the dermal collagen network, which is typically disrupted by the natural aging process of the skin. These findings not only corroborate existing data regarding the positive effects of oral collagen peptides on skin structure and function but also contribute to our understanding of ultrastructural morphological aspects of changes in the skin’s collagen network. Supplementation can induce regeneration of the collagen fiber network in the human skin. Trial Registration Number German Clinical Trials Register, DRKS-ID DRKS00034161- Date of registration: 06.05.2024, retrospectively registered.