State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China; Department of Rheumatology, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou 310003, China.
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.
Microbes Infect. 2024 Nov-Dec;26(8):105373. doi: 10.1016/j.micinf.2024.105373. Epub 2024 Jun 8.
Gut microbiota dysbiosis increases the susceptibility to Clostridioides difficile infection (CDI). In this study, we monitored C. difficile colonization (CDC) patients from no CDC status (CDN) to CDC status (CDCp) and CDI patients from asymptomatic status before CDI (PRECDI), CDI status (ONCDI), to asymptomatic status after CDI (POSTCDI). Based on metagenomic sequencing, we aimed to investigate the interaction pattern between gut microbiota and C. difficile. There was no significant difference of microbiota diversity between CDN and CDCp. In CDCp, Bacteroidetes and short-chain fatty acid (SCFA)-producing bacteria increased, with a positive correlation between SCFA-producing bacteria and C. difficile colonization. Compared with PRECDI, ONCDI and POSTCDI showed a significant decrease in microbiota diversity, particularly in Bacteroidetes and SCFA-producing bacteria, with a positive correlation between opportunistic pathogen and C. difficile. Fatty acid metabolism, and amino acid biosynthesis were enriched in CDN, CDCp, and PRECDI, while bile secretion was enriched in ONCDI and POSTCDI. Microbiota and metabolic pathways interaction networks in CDN and CDCp were more complex, particularly pathways in fatty acid and bile acid metabolism. Increasing of Bacteroidetes and SCFA-producing bacteria, affecting amino acid and fatty acid metabolism, is associated with colonization resistance to C. difficile and inhibiting the development of CDI.
肠道微生物失调增加了艰难梭菌感染（CDI）的易感性。在这项研究中，我们监测了从无艰难梭菌定植（CDN）到艰难梭菌定植（CDCp）的艰难梭菌定植（CDC）患者和无症状状态前 CDI（PRECDI）、CDI 状态（ONCDI）、CDI 后无症状状态（POSTCDI）的 CDI 患者。基于宏基因组测序，我们旨在研究肠道微生物群与艰难梭菌之间的相互作用模式。CDN 和 CDCp 之间的微生物多样性没有显著差异。在 CDCp 中，拟杆菌门和产生短链脂肪酸（SCFA）的细菌增加，与艰难梭菌定植呈正相关。与 PRECDI 相比，ONCDI 和 POSTCDI 的微生物多样性显著下降，尤其是拟杆菌门和产生 SCFA 的细菌，机会性病原体与艰难梭菌呈正相关。脂肪酸代谢和氨基酸生物合成在 CDN、CDCp 和 PRECDI 中富集，而胆汁分泌在 ONCDI 和 POSTCDI 中富集。CDN 和 CDCp 中的微生物群和代谢途径相互作用网络更复杂，尤其是脂肪酸和胆汁酸代谢途径。拟杆菌门和产生 SCFA 的细菌增加，影响氨基酸和脂肪酸代谢，与艰难梭菌定植抵抗和抑制 CDI 的发展有关。
