Scholarlink

<p>The progression of multiple sclerosis (MS) is potentially influenced by the microbiome. Elucidating host–microbiome interactions in MS may aid in developing microbiome-based applications; however, these interactions remain unclear. Here, we aimed to elucidate how <i>Veillonella ratti</i> MHL0042, isolated from human infant feces, modulates neuroinflammation and disease severity in experimental autoimmune encephalomyelitis, a murine MS model. Whole metagenomic sequencing revealed that <i>V. ratti</i> MHL0042 reshaped disrupted gut microbiota via microbial interactions throughout the intestinal tract. <i>V. ratti</i> MHL0042 administration significantly reduced central nervous system inflammation, notably decreasing CD4<sup>+</sup>IFN-γ⁺ T cell populations and activated spinal cord microglia. Mechanistically, <i>V. ratti</i> MHL0042 depleted <i>pldA</i>-containing bacteria, involved in phosphatidylethanolamine metabolism, thus elevating dioleoyl phosphatidylethanolamine (DOPE) levels. Increased DOPE was not only detected in the intestinal tract but also extended systemically and reflected in the central nervous system. Exogenous DOPE administration recapitulated the attenuation of experimental autoimmune encephalomyelitis pathogenesis by suppressing microglial activation. These findings highlight the therapeutic applicability of the microbiome and underscore its potential in human disease treatment.</p><p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Gut microbiome modulation by Veillonella ratti induces resistance to EAE pathogenesis via microbe-derived metabolites

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月14日

查看全文
  • Panida Sittipo,
  • Joon-Young Park,
  • Eunike Tiffany,
  • Ara Oh,
  • Subin Moon,
  • Chan Hee Lee,
  • Jae Sang Oh,
  • Tae-Young Kim,
  • Mi-Na Kweon,
  • Jaeseoung Choi,
  • Keon-Hyoung Song,
  • Dong-Woo Lee,
  • Myung Hee Nam,
  • Soo-Jong Hong,
  • Eun-Young Lee,
  • Seong Ran Jeon,
  • Ho-Yeon Song,
  • Bong-Soo Kim,
  • Yun Kyung Lee

摘要

The progression of multiple sclerosis (MS) is potentially influenced by the microbiome. Elucidating host–microbiome interactions in MS may aid in developing microbiome-based applications; however, these interactions remain unclear. Here, we aimed to elucidate how Veillonella ratti MHL0042, isolated from human infant feces, modulates neuroinflammation and disease severity in experimental autoimmune encephalomyelitis, a murine MS model. Whole metagenomic sequencing revealed that V. ratti MHL0042 reshaped disrupted gut microbiota via microbial interactions throughout the intestinal tract. V. ratti MHL0042 administration significantly reduced central nervous system inflammation, notably decreasing CD4+IFN-γ⁺ T cell populations and activated spinal cord microglia. Mechanistically, V. ratti MHL0042 depleted pldA-containing bacteria, involved in phosphatidylethanolamine metabolism, thus elevating dioleoyl phosphatidylethanolamine (DOPE) levels. Increased DOPE was not only detected in the intestinal tract but also extended systemically and reflected in the central nervous system. Exogenous DOPE administration recapitulated the attenuation of experimental autoimmune encephalomyelitis pathogenesis by suppressing microglial activation. These findings highlight the therapeutic applicability of the microbiome and underscore its potential in human disease treatment.