Scholarlink

<p>Alcohol-associated liver disease (ALD) has limited therapeutic options due to its complex pathogenesis. This study demonstrates the ALD-protective effects of extracellular nanoparticles derived from <i>Bifidobacterium bifidum</i> (BNPs), focusing on the concept of gut microbiota-derived nanoparticles (GNPs) in disease pathogenesis. When isolated BNPs were administered in an ALD mouse model, they upregulated Vsig4 receptor expression in liver macrophages, improving phagocytic clearance of harmful GNPs that contained bacterial DNA. GNPs activated liver inflammation via the cGAS-STING pathway, exacerbating ALD and liver fibrosis in Vsig4-deficient mice. BNP treatment suppressed the inflammatory cascade, modulated macrophage polarization, and reduced hepatic steatosis and liver injury, while also restoring the balance of the gut microbiota and enhancing intestinal barrier function. These findings reveal the role of GNPs in ALD pathogenesis and present targeted microbial nanoparticle postbiotics as potential therapeutics for treatment of alcohol-associated and other liver diseases.</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

Bifidobacterium bifidum-derived nanoparticles attenuate alcoholic liver disease via enhanced hepatic phagocytosis and gastrointestinal homeostasis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月30日

查看全文
  • Zelin Gu,
  • Shuhan Meng,
  • Boqing Yao,
  • Boya Gao,
  • Siye Chen,
  • Fazheng Ren,
  • Pinglan Li,
  • Tuo Shao,
  • Nan Shang

摘要

Alcohol-associated liver disease (ALD) has limited therapeutic options due to its complex pathogenesis. This study demonstrates the ALD-protective effects of extracellular nanoparticles derived from Bifidobacterium bifidum (BNPs), focusing on the concept of gut microbiota-derived nanoparticles (GNPs) in disease pathogenesis. When isolated BNPs were administered in an ALD mouse model, they upregulated Vsig4 receptor expression in liver macrophages, improving phagocytic clearance of harmful GNPs that contained bacterial DNA. GNPs activated liver inflammation via the cGAS-STING pathway, exacerbating ALD and liver fibrosis in Vsig4-deficient mice. BNP treatment suppressed the inflammatory cascade, modulated macrophage polarization, and reduced hepatic steatosis and liver injury, while also restoring the balance of the gut microbiota and enhancing intestinal barrier function. These findings reveal the role of GNPs in ALD pathogenesis and present targeted microbial nanoparticle postbiotics as potential therapeutics for treatment of alcohol-associated and other liver diseases.