ABSTRACT
Introduction
Atopic dermatitis (AD) is a common inflammatory cutaneous disease that arises due to dysregulation of the Th2 immune response, impaired skin barrier integrity, and dysbiosis of the skin and gut microbiota. An abundance of Staphylococcus aureus biofilms in AD lesions increases the Th2 immune response, and gut bacteria release breakdown products such as Short Chain Fatty Acids that regulate the systemic immune response.
Areas Covered
We aim to evaluate therapies that modulate the microbiome in humans and discuss the clinical implications of these treatments. We performed a review of the literature in which 2,673 records were screened, and describe the findings of 108 studies that were included after full-text review. All included studies discussed the effects of therapies on the human microbiome and AD severity. Oral probiotics, topical probiotics, biologics, and investigational therapies were included in our analysis.
Expert Opinion
Oral probiotics demonstrate mixed efficacy at relieving AD symptoms. Topical probiotics reduce S. aureus abundance in AD lesional skin, yet for moderate-severe disease, these therapies may not reduce AD severity scores to the standard of biologics. Dupilumab and tralokinumab target key inflammatory pathways in AD and modulate the skin microbiome, further improving disease severity.
Article highlights
Oral probiotics have varying levels of evidence for improving atopic dermatitis symptoms in infants, adults, and children.
Topical probiotics may reduce the abundance of Staphylococcus aureus on atopic dermatitis lesions and may improve atopic dermatitis symptoms.
Biologics such as dupilumab and tralokinumab are biologics that target the dysregulated immune system in atopic dermatitis, and they reduce S. aureus bacterial load on lesional skin.
Investigational therapies such as fecal microbial transplantation improve atopic dermatitis severity, although the data is to small experimental studies.
Declaration of interests
S Feldman has received research, speaking and/or consulting support from Eli Lilly and Company, GlaxoSmithKline/Stiefel, AbbVie, Janssen, Alovtech, vTv Therapeutics, Bristol-Myers Squibb, Samsung, Pfizer, Boehringer Ingelheim, Amgen, Dermavant, Arcutis, Novartis, Novan, UCB, Helsinn, Sun Pharma, Almirall, Galderma, Leo Pharma, Mylan, Celgene, Ortho Dermatology, Menlo, Merck & Co, Qurient, Forte, Arena, Biocon, Accordant, Argenx, Sanofi, Regeneron, the National Biological Corporation, Caremark, Teladoc, BMS, Ono, Micreos, Eurofins, Informa, UpToDate and the National Psoriasis Foundation. He is founder and part owner of Causa Research and holds stock in Sensal Health. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Reviewer disclosures
A reviewer on this manuscript has disclosed they have received honoraria for lectures from Sanofi Genzyme, Leo Pharma, Novartis, Norwegian Psoriasis and Eczema Association, and Norwegian Asthma and Allergy Association. Peer reviewers on this manuscript have no other relevant financial relationships or otherwise to disclose.
Supplementary material
Supplemental data for this article can be accessed online at https://doi.org/10.1080/13543784.2024.2326625