The Role of the Microbiome in Lichen Sclerosus: Pathophysiological Insights and Therapeutic Implications
- 1Department and Clinic of Dermatology, Sexually Transmitted Diseases and Clinical Immunology, University of Warmia and Mazury in Olsztyn, 10-229 Olsztyn Al. Wojska Polskiego 30, Olsztyn, Poland
- 2University of Warmia and Mazury in Olsztyn, Olsztyn, Poland
Abstract
Lichen sclerosus (LS) is a chronic inflammatory and fibrotic dermatosis of unclear etiology, traditionally considered an autoimmune disorder. Emerging evidence suggests that microbiome dysbiosis may contribute to disease pathogenesis by modulating local immune responses and tissue remodeling. This narrative review synthesizes current data on the skin, genital, and gut microbiome in LS, focusing on potential mechanistic links between microbial imbalance and immune activation. Available studies consistently show alterations in microbial composition; however, findings remain heterogeneous because of the small sample sizes, methodological variability, and predominantly cross-sectional designs. Despite these limitations, accumulating data indicate that microbial dysbiosis may influence key immunological pathways involved in LS, including T-cell activation and chronic inflammation. In particular, mucosa-associated invariant T (MAIT) cells are proposed as a potential mechanistic bridge between microbial-derived signals and immune dysregulation, although their role in LS remains unclear. These observations support a conceptual model of LS as a microbiome-modulated inflammatory and fibrotic disorder rather than a purely autoimmune condition. Clinically, microbiome profiling and targeted modulation may offer novel diagnostic and therapeutic opportunities. Future research should prioritize longitudinal and interventional studies, ideally incorporating multi-omics approaches, to clarify causality and facilitate translation into clinical practice.
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BibTeX
@article{kasprowiczfurmanczyk2026role,
title = {{The Role of the Microbiome in Lichen Sclerosus: Pathophysiological Insights and Therapeutic Implications}},
author = {Marta Kasprowicz-Furmańczyk and Witold Chmielnicki and Natalia Zdanowska and Agnieszka Owczarczyk-Saczonek},
journal = {Dermatology and Therapy},
year = {2026},
month = sep,
doi = {10.1007/s13555-026-01923-7},
url = {https://doi.org/10.1007/s13555-026-01923-7},
note = {CC BY-NC 4.0},
}
RIS
TY - JOUR
TI - The Role of the Microbiome in Lichen Sclerosus: Pathophysiological Insights and Therapeutic Implications
AU - Marta Kasprowicz-Furmańczyk
AU - Witold Chmielnicki
AU - Natalia Zdanowska
AU - Agnieszka Owczarczyk-Saczonek
PY - 2026
DA - 2026/09/01
JO - Dermatology and Therapy
DO - 10.1007/s13555-026-01923-7
UR - https://doi.org/10.1007/s13555-026-01923-7
AB - Lichen sclerosus (LS) is a chronic inflammatory and fibrotic dermatosis of unclear etiology, traditionally considered an autoimmune disorder. Emerging evidence suggests that microbiome dysbiosis may contribute to disease pathogenesis by modulating local immune responses and tissue remodeling. This narrative review synthesizes current data on the skin, genital, and gut microbiome in LS, focusing on potential mechanistic links between microbial imbalance and immune activation. Available studies consistently show alterations in microbial composition; however, findings remain heterogeneous because of the small sample sizes, methodological variability, and predominantly cross-sectional designs. Despite these limitations, accumulating data indicate that microbial dysbiosis may influence key immunological pathways involved in LS, including T-cell activation and chronic inflammation. In particular, mucosa-associated invariant T (MAIT) cells are proposed as a potential mechanistic bridge between microbial-derived signals and immune dysregulation, although their role in LS remains unclear. These observations support a conceptual model of LS as a microbiome-modulated inflammatory and fibrotic disorder rather than a purely autoimmune condition. Clinically, microbiome profiling and targeted modulation may offer novel diagnostic and therapeutic opportunities. Future research should prioritize longitudinal and interventional studies, ideally incorporating multi-omics approaches, to clarify causality and facilitate translation into clinical practice.
SN - 2193-8210
SN - 2190-9172
ER -