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<p>The infant gut microbiota is essential for immune development, yet its disruption in eczema remains poorly understood. In this cross-sectional study, we compared the gut microbiota and faecal metabolites of infants with eczema and healthy controls and used in vitro fermentation to assess microbial metabolic activity and substrate-dependent responses. Infants with eczema showed depletion of acidogenic and acidophilic bacteria, including <i>Enterococcus faecium</i>, <i>Citrobacter</i>, and <i>Streptococcus</i> unclassified, together with decreased absolute counts of <i>Lactobacillus</i>, reduced total bile acids, and altered short-chain fatty acid profiles. In vitro fermentation reproduced several group-specific microbial differences, although their extent varied among substrates; <i>Escherichia-Shigella</i>, <i>E. coli</i>, <i>Citrobacter</i>, <i>Clostridium butyricum</i>, and the <i>[Ruminococcus] gnavus</i> group were more frequently enriched in controls than in the eczema group. Based on these findings, we propose a Dual Driving Force Hypothesis of infant gut microbiota succession, in which early-life lactate accumulation favours acidogenic and acid-tolerant bacteria, whereas subsequent bile acid maturation provides a secondary ecological driver of microbiota development. Disruption of this sequential process may impair microbial succession and immune maturation. Our findings provide evidence of impaired intestinal acidification in infantile eczema, are consistent with the hygiene hypothesis, and suggest a conceptual basis for microbiome-targeted prevention strategies.</p>

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Gut acidification impairment links altered acidogenic microbiota to infantile eczema: a cross-sectional study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月25日

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  • Huiwen Zheng,
  • Yin Li,
  • Wei Li,
  • Xiaoxuan Guo,
  • Chunlan Huang,
  • Sha Zhou,
  • Zhen Wang,
  • Chen Chen,
  • Lifei Hu,
  • Jinjun Li,
  • Xiaoqiong Li,
  • Yunling Li,
  • Liying Zhu

摘要

The infant gut microbiota is essential for immune development, yet its disruption in eczema remains poorly understood. In this cross-sectional study, we compared the gut microbiota and faecal metabolites of infants with eczema and healthy controls and used in vitro fermentation to assess microbial metabolic activity and substrate-dependent responses. Infants with eczema showed depletion of acidogenic and acidophilic bacteria, including Enterococcus faecium, Citrobacter, and Streptococcus unclassified, together with decreased absolute counts of Lactobacillus, reduced total bile acids, and altered short-chain fatty acid profiles. In vitro fermentation reproduced several group-specific microbial differences, although their extent varied among substrates; Escherichia-Shigella, E. coli, Citrobacter, Clostridium butyricum, and the [Ruminococcus] gnavus group were more frequently enriched in controls than in the eczema group. Based on these findings, we propose a Dual Driving Force Hypothesis of infant gut microbiota succession, in which early-life lactate accumulation favours acidogenic and acid-tolerant bacteria, whereas subsequent bile acid maturation provides a secondary ecological driver of microbiota development. Disruption of this sequential process may impair microbial succession and immune maturation. Our findings provide evidence of impaired intestinal acidification in infantile eczema, are consistent with the hygiene hypothesis, and suggest a conceptual basis for microbiome-targeted prevention strategies.