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<p><i>Campylobacter</i> infections are a leading cause of acute infectious gastroenteritis, associated with the development of post-infection irritable bowel syndrome (PI-IBS). Host characteristics like biological sex, age, psychosocial factors and enteritis severity associate with PI-IBS development. Immortalized cell lines have described <i>Campylobacter</i> infection; yet these models fail to recapitulate the complexity of human epithelia and the variability of host factors. Here, we use colonic organoids derived from high and low anxiety/depression, female and male volunteers, to assess how host demographics influence responses to <i>Campylobacter</i> infection. <i>C. jejuni</i> demonstrated the ability to infect human colonoid monolayers. Greater bacterial attachment to colonoids from volunteers defined as high anxiety and depression (AD) was observed compared to low AD. Barrier loss was greater in high AD organoid monolayers compared to low AD after infection with the breakdown of tight junction proteins occludin and ZO-1. Transcriptomic profiling showed high AD organoids had upregulation of CXCL10 and CXCL11, mucins (MUC2, MUC5AC, and MUC6) and host proteases (PRSS3P1 and PRSS1) compared to low AD. These findings show the utility of colonoids for studying <i>C. jejuni</i> infectivity, highlighting variability in molecular responses based on host demographics. Studies incorporating human colonic organoid cultures will help inform host-bacteria interactions and personalized host responses leading to the development of gastrointestinal disease.</p>

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Human colonic organoid monolayers reveal biological sex and psychological state influence epithelial responses to Campylobacter jejuni infection

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月6日

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  • Adam Edwinson,
  • Stephanie Peters,
  • Margaret Breen-Lyles,
  • Ryan J. Lennon,
  • Surendra Dasari,
  • Madhusudan Grover

摘要

Campylobacter infections are a leading cause of acute infectious gastroenteritis, associated with the development of post-infection irritable bowel syndrome (PI-IBS). Host characteristics like biological sex, age, psychosocial factors and enteritis severity associate with PI-IBS development. Immortalized cell lines have described Campylobacter infection; yet these models fail to recapitulate the complexity of human epithelia and the variability of host factors. Here, we use colonic organoids derived from high and low anxiety/depression, female and male volunteers, to assess how host demographics influence responses to Campylobacter infection. C. jejuni demonstrated the ability to infect human colonoid monolayers. Greater bacterial attachment to colonoids from volunteers defined as high anxiety and depression (AD) was observed compared to low AD. Barrier loss was greater in high AD organoid monolayers compared to low AD after infection with the breakdown of tight junction proteins occludin and ZO-1. Transcriptomic profiling showed high AD organoids had upregulation of CXCL10 and CXCL11, mucins (MUC2, MUC5AC, and MUC6) and host proteases (PRSS3P1 and PRSS1) compared to low AD. These findings show the utility of colonoids for studying C. jejuni infectivity, highlighting variability in molecular responses based on host demographics. Studies incorporating human colonic organoid cultures will help inform host-bacteria interactions and personalized host responses leading to the development of gastrointestinal disease.