Background <p>Bacterial associations with fungal hosts are increasingly recognized as common rather than exceptional. Among these interactions, Candida spp. and Helicobacter pylori are of particular interest, as evidence suggests that Candida may serve as a potential host for H. pylori, facilitating its persistence and dissemination. Although interactions between Candida spp. and members of the bacterial microbiota—particularly H. pylori—are increasingly recognized for their role in modulating microbial ecology and influencing pathological outcomes in the host, the impact of H. pylori on Candida albicans remains poorly characterized. Whether this interaction alters the biological behavior or pathogenic potential of Candida spp. remains poorly understood. In this study, C. albicans strains CacoHp, which were detected to be positive for H. pylori–specific genes, were generated through co-culture, and the effects of this bacterial–fungal interaction on tolerance and virulence were investigated.</p> Results <p>Co-culture with H. pylori S7 and C. albicans SC5314 yielded Hp-positive C. albicans CacoHp. Compared with the parental strain SC5314, CacoHp exhibited increased tolerance to antifungal agents, sodium dodecyl sulfate, and H<sub>2</sub>O<sub>2</sub>; enhanced inhibition of GES-1 cell proliferation; elevated aspartic protease secretion; and increased hyphal formation. Proteomic and quantitative polymerase chain reaction analyses indicated upregulation of ergosterol transport (SNQ2) and vacuolar ATPase (VMA8) pathways, and enhanced stress tolerance. In mice, CacoHp induced a stronger inflammatory response and more severe gastric tissue damage than the SC5314 strain.</p> Conclusions <p>Co-culture with H. pylori generates C. albicans strains CacoHp, which were detected to be positive for H. pylori–specific genes, that exhibit enhanced chemical stress tolerance and increased virulence. This study first revealed the influence of H. pylori on Candida phenotypes, further supporting the clinical relevance of their interaction.</p>

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Association of Helicobacter pylori with Candida albicans enhances fungal virulence and stress tolerance

  • Jianchao Sun,
  • Qing Luo,
  • Tingxiu Yang,
  • Xiaoli Xu,
  • Tingting Luo,
  • Huifeng Jian,
  • Xianli Chen,
  • Guzhen Cui,
  • Zhenghong Chen

摘要

Background

Bacterial associations with fungal hosts are increasingly recognized as common rather than exceptional. Among these interactions, Candida spp. and Helicobacter pylori are of particular interest, as evidence suggests that Candida may serve as a potential host for H. pylori, facilitating its persistence and dissemination. Although interactions between Candida spp. and members of the bacterial microbiota—particularly H. pylori—are increasingly recognized for their role in modulating microbial ecology and influencing pathological outcomes in the host, the impact of H. pylori on Candida albicans remains poorly characterized. Whether this interaction alters the biological behavior or pathogenic potential of Candida spp. remains poorly understood. In this study, C. albicans strains CacoHp, which were detected to be positive for H. pylori–specific genes, were generated through co-culture, and the effects of this bacterial–fungal interaction on tolerance and virulence were investigated.

Results

Co-culture with H. pylori S7 and C. albicans SC5314 yielded Hp-positive C. albicans CacoHp. Compared with the parental strain SC5314, CacoHp exhibited increased tolerance to antifungal agents, sodium dodecyl sulfate, and H2O2; enhanced inhibition of GES-1 cell proliferation; elevated aspartic protease secretion; and increased hyphal formation. Proteomic and quantitative polymerase chain reaction analyses indicated upregulation of ergosterol transport (SNQ2) and vacuolar ATPase (VMA8) pathways, and enhanced stress tolerance. In mice, CacoHp induced a stronger inflammatory response and more severe gastric tissue damage than the SC5314 strain.

Conclusions

Co-culture with H. pylori generates C. albicans strains CacoHp, which were detected to be positive for H. pylori–specific genes, that exhibit enhanced chemical stress tolerance and increased virulence. This study first revealed the influence of H. pylori on Candida phenotypes, further supporting the clinical relevance of their interaction.