: The ineffective combination of corticosteroids and antibiotics in treating some atopic dermatitis (AD) cases has been concerning. The skin barrier defects in AD ease the colonization of (), which results in a rise in interleukin-31 (IL-31). () has shown antimicrobial and antiallergic effects but has not been studied yet to decrease the growth of and IL-31 levels in AD patients. This study aimed to analyze the effect of extract in reducing colonization, the IL-31 level, and the severity of AD. : A randomized controlled trial (RCT) (international registration number TCTR20231025004) was conducted on 40 AD patients attending Dermatology and Venereology Polyclinic, Mother and Child Hospital (RSIA), Aceh, Indonesia, from October 2021 to March 2022. AD patients aged 8-16 who had a Scoring Atopic Dermatitis (SCORAD) index > 25, with total IgE serum level > 100 IU/mL, and had healthy weight were randomly assigned into two groups: one received fluocinolone acetonide 0.025% and placebo (control group) and one received fluocinolone acetonide 0.025% combined with extract (Vermint) (intervention group). The colony was identified using a catalase test, coagulase test, and MSA media. The serum IL-31 levels were measured using ELISA assay, while the SCORAD index was used to assess the severity of and improvement in AD. Mean scores for measured variables were compared between the two groups using an unpaired t-test and Mann-Whitney U test. : A significant decline in colonization ( = 0.001) and IL-31 ( = 0.013) in patients receiving extract was found in this study. Moreover, fourteen AD patients in the intervention group showed an improvement in the SCORAD index of more than 35% ( = 0.057). : extract significantly decreases colonization and the IL-31 level in AD patients, suggesting its potential as an adjuvant therapy for children with AD.
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http://dx.doi.org/10.3390/medicina59112007 | DOI Listing |
Medicina (Kaunas)
November 2023
Department of Microbiology, Faculty of Medicine, Universitas Syiah Kuala, Banda Aceh 23111, Indonesia.
: The ineffective combination of corticosteroids and antibiotics in treating some atopic dermatitis (AD) cases has been concerning. The skin barrier defects in AD ease the colonization of (), which results in a rise in interleukin-31 (IL-31). () has shown antimicrobial and antiallergic effects but has not been studied yet to decrease the growth of and IL-31 levels in AD patients.
View Article and Find Full Text PDFFront Mol Biosci
August 2023
Department of Dermatology-Venereology and Allergology, Universitätsklinikum Schleswig-Holstein, Kiel, Germany.
Atopic dermatitis (AD) is a common, chronic and relapsing inflammatory skin disease with various clinical presentations and combinations of symptoms. The pathophysiology of AD is complex and multifactorial. There are several factors involved in the etiopathogenesis of AD including structural and immunological epidermal barrier defect, imbalance of the skin microbiome, genetic background and environmental factors.
View Article and Find Full Text PDFFront Immunol
March 2023
Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Republic of Korea.
Introduction & Objectives: Head and neck dermatitis (HND) is a refractory phenotype of atopic dermatitis (AD) and can be a therapeutic challenge due to lack of responsiveness to conventional treatments. Previous studies have suggested that the microbiome and fungiome may play a role in inducing HND, but the underlying pathogenic mechanisms remain unknown. This study aimed to determine the link between HND and fungiome and to examine the contribution of .
View Article and Find Full Text PDFJID Innov
September 2022
Sanofi, Cambridge, Massachusetts, USA.
Skin barrier dysfunction, a defining feature of atopic dermatitis (AD), arises from multiple interacting systems. In AD, skin inflammation is caused by host-environment interactions involving keratinocytes as well as tissue-resident immune cells such as type 2 innate lymphoid cells, basophils, mast cells, and T helper type 2 cells, which produce type 2 cytokines, including IL-4, IL-5, IL-13, and IL-31. Type 2 inflammation broadly impacts the expression of genes relevant for barrier function, such as intracellular structural proteins, extracellular lipids, and junctional proteins, and enhances skin colonization.
View Article and Find Full Text PDFBiol Pharm Bull
November 2021
Department of Clinical Immunology, Meiji Pharmaceutical University.
Our previous study showed that chronic skin colonization by Staphylococcus aureus exacerbated atopic dermatitis (AD) and that control of such skin colonization using antibiotic ointment might relieve AD-related skin inflammation. However, the role of S. aureus colonization in the pruritus accompanying AD was not elucidated.
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