Hu Suhui, Liu Zhenzhen, Yan Wenchao, Guo Rongxian
College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, China.
PLoS Pathog. 2025 Sep 11;21(9):e1013494. doi: 10.1371/journal.ppat.1013494. eCollection 2025 Sep.
The interactions between bacterial pathogens, helminths, and commensal microbiota in the gut form a complex ecological network that profoundly impacts host immunity and health. Pathogens employ strategies such as type VI secretion systems (T6SS) and inflammation induction to evade colonization resistance, disrupt microbial balance, and establish self-benefit ecological niches. These interactions involve competition with commensal bacteria and helminths, which play a critical role in maintaining gut homeostasis by occupying ecological niches, competing for nutrient, and supporting the mucus barrier. Meanwhile, helminths can modulate commensal bacterial gene expression, metabolic activity, and survival by secreting excretory-secretory products. In addition, by inducing a Th2 immune response, helminths can enhance the intestinal mucosal barrier, alter the gut microbiota composition, and thereby inhibit bacterial pathogen colonization. Interestingly, helminths and pathogens can exhibit synergistic or competitive relationships. For instance, Ascaris lumbricoides may provide a survival niche for Vibrio cholerae, while helminths can also indirectly inhibit pathogenic bacteria through immune modulation. These intricate interactions influence gut microbial composition, digestion, and immune function, and are closely associated with diseases. Future research should focus on elucidating the molecular mechanisms underlying these interactions. Understanding the interactions between pathogens, helminths, and commensal microbiota not only provides novel insights into maintaining host immune homeostasis but also establishes a theoretical foundation for future development of gut health intervention strategies.
肠道中细菌病原体、蠕虫和共生微生物群之间的相互作用形成了一个复杂的生态网络,对宿主免疫和健康产生深远影响。病原体采用如VI型分泌系统(T6SS)和诱导炎症等策略来逃避定植抗性、破坏微生物平衡并建立有利于自身的生态位。这些相互作用涉及与共生细菌和蠕虫的竞争,共生细菌和蠕虫通过占据生态位、争夺营养和支持黏液屏障在维持肠道稳态中发挥关键作用。同时,蠕虫可通过分泌排泄-分泌产物来调节共生细菌的基因表达、代谢活性和存活。此外,通过诱导Th2免疫反应,蠕虫可增强肠道黏膜屏障、改变肠道微生物群组成,从而抑制细菌病原体定植。有趣的是,蠕虫和病原体可表现出协同或竞争关系。例如,蛔虫可能为霍乱弧菌提供生存 niche,而蠕虫也可通过免疫调节间接抑制病原菌。这些复杂的相互作用影响肠道微生物组成、消化和免疫功能,并与疾病密切相关。未来的研究应侧重于阐明这些相互作用背后的分子机制。了解病原体、蠕虫和共生微生物群之间的相互作用不仅为维持宿主免疫稳态提供了新的见解,也为未来肠道健康干预策略的发展奠定了理论基础。