Abstract

The etiology of vulvar lichen sclerosus (LS) remains unclear; however, alterations in cutaneous and gut microbiota may be contributing to the pathogenesis of this inflammatory condition. To explore this hypothesis, we conducted a pilot case-control study, obtaining dermal swab and stool samples from prepubertal girls with vulvar LS (n = 5), girls with nonspecific vulvovaginitis (n = 5), and healthy controls (n = 3). Samples (n = 56) were subjected to total DNA extractions. Resulting DNA was purified, subjected to PCR (targeting the V3V4 region of the 16S rRNA gene), sequenced, and analyzed using QIIME, MetagenomeSeq, and DESeq2 software packages. Our findings showed that there were significant differences in the cutaneous and gut microbiotas of girls with LS compared to controls. On the skin, girls with LS had a statistically significantly higher relative abundance of Porphyromonas spp., Parvimonas spp., Peptoniphilus spp., Prevotella spp., Dialister spp., and Peptostreptococcus spp., but a lower relative abundance of Cornyebacterium compared to the control group. In the gut samples, girls with LS had a significantly higher relative abundance of Dialister spp., Clostridiales spp., Paraprevotella spp., Escherichia coli, Bifidobacterium adolescentis, and Akkermansia muciniphila, and a lower relative abundance of Roseburia faecis and Ruminococcus bromii compared to controls. These results suggest a potential association between cutaneous and gut dysbiosis and pediatric vulvar LS. Future studies involving larger samples sizes are warranted to further evaluate this association.

Highlights

  • Lichen sclerosus (LS) is a chronic inflammatory skin condition that presents as painful, pruritic, ivory-white atrophic patches, most commonly within the genital region of premenarchal girls or post-menopausal women [1]

  • S. aureus is more prevalent on the skin of infants preceding the development of atopic dermatitis compared to age-matched unaffected infants, suggesting that S. aureus colonization contributes to the onset of atopic dermatitis and is not a result of the disease [10]

  • We demonstrated that girls with LS have a higher relative abundance of Dialister spp. in the gut, which is consistent with findings from other inflammatory diseases [22]

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Summary

Introduction

Lichen sclerosus (LS) is a chronic inflammatory skin condition that presents as painful, pruritic, ivory-white atrophic patches, most commonly within the genital region of premenarchal girls or post-menopausal women [1]. Immunologic, and hormonal factors have been implicated in the pathogenesis of LS, the exact etiology of LS remains unclear [3, 4]. Local factors such as the skin microbiota have been proposed as possible causes to LS, as vulvar skin with LS becomes normal when transplanted to the thigh, and normal skin transplanted to the affected vulva develops LS [5]. The skin microbiota likely contributes to the development of dermatologic diseases by disrupting the skin barrier and dysregulating the immune system. S. aureus is more prevalent on the skin of infants preceding the development of atopic dermatitis compared to age-matched unaffected infants, suggesting that S. aureus colonization contributes to the onset of atopic dermatitis and is not a result of the disease [10]

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