Department of Urology, Chung-Ang University College of Medicine, 84 Heukseok-ro, Dongjak-gu, Seoul, 06974, Republic of Korea.
Advanced Urogenital Diseases Research Center, Chung-Ang University College of Medicine, 84 Heukseok-ro, Dongjak-gu, Seoul, 06974, Republic of Korea.
Probiotics Antimicrob Proteins. 2017 Dec;9(4):406-414. doi: 10.1007/s12602-017-9286-6.
Vaginal commensal lactobacilli are considered to contribute significantly to the control of vaginal microbiota by competing with other microflora for adherence to the vaginal epithelium and by producing antimicrobial compounds. However, the molecular mechanisms of symbiotic prokaryotic-eukaryotic communication in the vaginal ecosystem remain poorly understood. Here, we showed that both DNA methylation and histone modifications were associated with expression of the DEFB1 gene, which encodes the antimicrobial peptide human β-defensin-1, in vaginal keratinocyte VK2/E6E7 cells. We investigated whether exposure to Lactobacillus gasseri and Lactobacillus reuteri would trigger the epigenetic modulation of DEFB1 expression in VK2/E6E7 cells in a bacterial species-dependent manner. While enhanced expression of DEFB1 was observed when VK2/E6E7 cells were exposed to L. gasseri, treatment with L. reuteri resulted in reduced DEFB1 expression. Moreover, L. gasseri stimulated the recruitment of active histone marks and, in contrast, L. reuteri led to the decrease of active histone marks at the DEFB1 promoter. It was remarkable that distinct histone modifications within the same promoter region of DEFB1 were mediated by L. gasseri and L. reuteri. Therefore, our study suggested that one of the underlying mechanisms of DEFB1 expression in the vaginal ecosystem might be associated with the epigenetic crosstalk between individual Lactobacillus spp. and vaginal keratinocytes.
阴道共生乳杆菌被认为通过与其他微生物争夺对阴道上皮的附着以及产生抗菌化合物来显著控制阴道微生物群。然而,阴道生态系统中共生原核生物-真核生物通讯的分子机制仍知之甚少。在这里,我们表明,DNA 甲基化和组蛋白修饰都与编码抗菌肽人β-防御素-1 的 DEFB1 基因的表达相关,该基因在阴道角质形成细胞 VK2/E6E7 细胞中。我们研究了乳酸杆菌和罗伊氏乳杆菌暴露是否会以细菌物种依赖的方式触发 VK2/E6E7 细胞中 DEFB1 表达的表观遗传调节。虽然当 VK2/E6E7 细胞暴露于 L. gasseri 时观察到 DEFB1 的表达增强,但用 L. reuteri 处理会导致 DEFB1 表达减少。此外,L. gasseri 刺激活性组蛋白标记的募集,而相反,L. reuteri 导致 DEFB1 启动子处的活性组蛋白标记减少。值得注意的是,DEFB1 基因启动子内相同区域的不同组蛋白修饰是由 L. gasseri 和 L. reuteri 介导的。因此,我们的研究表明,阴道生态系统中 DEFB1 表达的潜在机制之一可能与个体乳杆菌和阴道角质形成细胞之间的表观遗传串扰有关。