鸟氨酸
免疫系统
微生物学
生物
分泌物
失调
精氨酸
肠粘膜
发病机制
肠道菌群
免疫学
医学
生物化学
内科学
氨基酸
作者
Huan Yang,Xiaoxiao Wu,Li Xiao,Wanqing Zang,Zhou Zhou,Yuan Zhou,Wenwen Cui,Yanbo Kou,Liang Wang,Ankang Hu,Lianlian Wu,Zhinan Yin,Quangang Chen,Y Chen,Zhutao Huang,Yugang Wang,Bingchuan Gu
标识
DOI:10.1038/s41467-024-47075-0
摘要
Antibiotic-induced dysbiosis is a major risk factor for Clostridioides difficile infection (CDI), and fecal microbiota transplantation (FMT) is recommended for treating CDI. However, the underlying mechanisms remain unclear. Here, we show that Tritrichomonas musculis (T.mu), an integral member of the mouse gut commensal microbiota, reduces CDI-induced intestinal damage by inhibiting neutrophil recruitment and IL-1β secretion, while promoting Th1 cell differentiation and IFN-γ secretion, which in turn enhances goblet cell production and mucin secretion to protect the intestinal mucosa. T.mu can actively metabolize arginine, not only influencing the host's arginine-ornithine metabolic pathway, but also shaping the metabolic environment for the microbial community in the host's intestinal lumen. This leads to a relatively low ornithine state in the intestinal lumen in C. difficile-infected mice. These changes modulate C. difficile's virulence and the host intestinal immune response, and thus collectively alleviating CDI. These findings strongly suggest interactions between an intestinal commensal eukaryote, a pathogenic bacterium, and the host immune system via inter-related arginine-ornithine metabolism in the regulation of pathogenesis and provide further insights for treating CDI.
科研通智能强力驱动
Strongly Powered by AbleSci AI