Scholarlink

<p>Ulcerative colitis (UC) is a chronic, recurrent inflammatory bowel disease (IBD) marked by inflammation of the colonic mucosa. While its precise aetiology remains unclear, emerging evidence underscores the pivotal role of gut microbiota in UC pathogenesis. In healthy individuals, the gut microbiota contributes to immune modulation, nutrient absorption, and maintenance of intestinal barrier integrity. In contrast, individuals with UC exhibit gut dysbiosis—characterized by a reduction in beneficial bacteria such as <i>Faecalibacterium prausnitzii</i> and <i>Bifidobacterium</i>, and an increase in potentially pathogenic microbes like <i>Escherichia coli</i>. This microbial imbalance disrupts mucosal homeostasis, promotes persistent inflammation, and impairs epithelial healing. Contributing factors include genetic predisposition, antibiotic exposure, diet, and environmental influences. Novel microbiota-targeted interventions—such as probiotics, prebiotics, dietary modifications, and faecal microbiota transplantation (FMT)—are being actively explored, with promising preliminary outcomes in symptom relief and microbiome restoration. However, challenges persist in defining a “healthy” microbiome and standardizing therapeutic protocols. This study highlights the potential of microbiome modulation as a transformative approach in UC management and calls for further research into host-microbe interactions to advance precision-based, microbiota-oriented therapies.</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

The gut immune axis in ulcerative colitis: insights from microbiome research

  • 期刊论文

  • 发表日期：

    2025年10月10日

查看全文
  • Rufaida Wasim

摘要

Ulcerative colitis (UC) is a chronic, recurrent inflammatory bowel disease (IBD) marked by inflammation of the colonic mucosa. While its precise aetiology remains unclear, emerging evidence underscores the pivotal role of gut microbiota in UC pathogenesis. In healthy individuals, the gut microbiota contributes to immune modulation, nutrient absorption, and maintenance of intestinal barrier integrity. In contrast, individuals with UC exhibit gut dysbiosis—characterized by a reduction in beneficial bacteria such as Faecalibacterium prausnitzii and Bifidobacterium, and an increase in potentially pathogenic microbes like Escherichia coli. This microbial imbalance disrupts mucosal homeostasis, promotes persistent inflammation, and impairs epithelial healing. Contributing factors include genetic predisposition, antibiotic exposure, diet, and environmental influences. Novel microbiota-targeted interventions—such as probiotics, prebiotics, dietary modifications, and faecal microbiota transplantation (FMT)—are being actively explored, with promising preliminary outcomes in symptom relief and microbiome restoration. However, challenges persist in defining a “healthy” microbiome and standardizing therapeutic protocols. This study highlights the potential of microbiome modulation as a transformative approach in UC management and calls for further research into host-microbe interactions to advance precision-based, microbiota-oriented therapies.