Abstract

Human beta defensins (hBDs) may play an important role in the progression of lichen sclerosus (LS), due to their ability to induce excessive stimulation of extracellular matrix synthesis and fibroblast activation. The genetic ability of the individual to produce defensins, the presence of microbes influencing defensin production, and the sensitivity of microbes to defensins together regulate the formation of an ever-changing balance between defensin levels and microbiome composition. We investigated the potential differences in postmenopausal vaginal microbiome composition and vaginal hBD levels in LS patients compared to non-LS controls. LS patients exhibited significantly lower levels of hBD1 (p = 0.0003), and significantly higher levels of hBD2 (p = 0.0359) and hBD3 (p = 0.0002), compared to the control group. The microbiome of the LS patients was dominated by possibly harmful bacteria including Lactobacillus iners, Streptococcus anginosus or Gardnerella vaginalis known to initiate direct or indirect damage by increasing defensin level production. Our observations highlight that correcting the composition of the microbiome may be applicable in supplementary LS therapy by targeting the restoration of the beneficial flora that does not increase hBD2-3 production.

Highlights

  • Human beta defensins may play an important role in the progression of lichen sclerosus (LS), due to their ability to induce excessive stimulation of extracellular matrix synthesis and fibroblast activation

  • Β-defensins are subdivided into further subgroups: hBD1 is produced in the kidney, in the epithelial cells of the respiratory tract and in the female genital tract constitutively, while hBD2 and hBD3 are inducible, expressed in inflammatory diseases of the skin

  • We aimed to investigate postmenopausal vaginal microbiome and associated defensin levels in LS and control patients

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Summary

Introduction

Human beta defensins (hBDs) may play an important role in the progression of lichen sclerosus (LS), due to their ability to induce excessive stimulation of extracellular matrix synthesis and fibroblast activation. The microbiome of the LS patients was dominated by possibly harmful bacteria including Lactobacillus iners, Streptococcus anginosus or Gardnerella vaginalis known to initiate direct or indirect damage by increasing defensin level production. Β-defensins are subdivided into further subgroups: hBD1 is produced in the kidney, in the epithelial cells of the respiratory tract and in the female genital tract constitutively, while hBD2 and hBD3 are inducible, expressed in inflammatory diseases of the skin. In addition to their known antibacterial activity, they contribute to immunomodulatory and chemotactic effects in inflammatory processes, infections and wound h

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