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<p><i>Candida albicans</i> is a common gut commensal, typically restricted by the resident microbiota. However, microbiome disruption can enable its outgrowth, increasing the risk of life-threatening candidiasis. Restoring key protective microbes offer a therapeutic strategy, though their identification remains challenging. Using the M-SHIME® model simulating the human proximal colon, we investigated <i>C. albicans</i>-bacteriome interactions under eubiotic and dysbiotic conditions. We assessed how clindamycin, ciprofloxacin, and metronidazole modulate <i>C. albicans</i> colonization and evaluated associated microbial and metabolic shifts. The effects were antibiotic- and donor-specific: clindamycin facilitated colonization, ciprofloxacin had no impact, and metronidazole showed variable outcomes. Engraftment did not correlate with total bacterial concentration or α-diversity, but with the loss of specific taxa, notably <i>Lachnospiraceae</i> and <i>Bifidobacterium</i>. These correlations were supported functionally by reductions in acetate and butyrate, suggesting a metabolic mechanism of fungal suppression. This study highlights the role of dysbiosis in <i>C. albicans</i> outgrowth and supports targeted microbiome restoration strategies.</p>

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Candida albicans colonization in the human colon correlates with a reduction in acetate- and butyrate-producing bacteria, as simulated using the M-SHIME® model

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月26日

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  • Benoît Marsaux,
  • Warre d’Hoker,
  • Frédéric Moens,
  • Dries Van Elst,
  • Yorick Minnebo,
  • Massimo Marzorati,
  • Tom Van de Wiele

摘要

Candida albicans is a common gut commensal, typically restricted by the resident microbiota. However, microbiome disruption can enable its outgrowth, increasing the risk of life-threatening candidiasis. Restoring key protective microbes offer a therapeutic strategy, though their identification remains challenging. Using the M-SHIME® model simulating the human proximal colon, we investigated C. albicans-bacteriome interactions under eubiotic and dysbiotic conditions. We assessed how clindamycin, ciprofloxacin, and metronidazole modulate C. albicans colonization and evaluated associated microbial and metabolic shifts. The effects were antibiotic- and donor-specific: clindamycin facilitated colonization, ciprofloxacin had no impact, and metronidazole showed variable outcomes. Engraftment did not correlate with total bacterial concentration or α-diversity, but with the loss of specific taxa, notably Lachnospiraceae and Bifidobacterium. These correlations were supported functionally by reductions in acetate and butyrate, suggesting a metabolic mechanism of fungal suppression. This study highlights the role of dysbiosis in C. albicans outgrowth and supports targeted microbiome restoration strategies.