Our current understanding of the host-microbiota interaction in the gut is dominated by studies focused primarily on prokaryotic bacterial communities. However, there is an underappreciated symbiotic eukaryotic protistic community that is an integral part of mammalian microbiota. How commensal protozoan-bacteria might interact to form a stable microbial community remains poorly understood. Here, we described a murine protistic commensal phylogenetically assigned as Tritrichomonas musculis, whose colonization in the gut resulted in a reduction of gut bacterial abundance and diversity in wild-type C57BL/6 mice. Meanwhile, dietary nutrient and commensal bacteria also influenced the protozoan's intestinal colonization and stability. While mice fed on normal chow diet had abundant T. musculis, switching to a Western-type high-fat diet led to the diminishment of the protozoan from the gut. Supplementation of inulin as a dietary fiber to the high-fat diet partially restored the protozoan's colonization. In addition, a cocktail of broad-spectrum antibiotics rendered permissive engraftment of T. musculis even under a high-fat low-fiber diet condition. Furthermore, oral administration of Bifidobacterium spp. together with dietary supplementation of inulin in the high-fat diet impacted the protozoan's intestinal engraftment in a bifidobacterial species-dependent manner. Overall, our study described an example of dietary nutrient-dependent murine commensal protozoan-bacteria crosstalk as an important modulator of the host intestinal microbiome.

Importance: Like commensal bacteria, commensal protozoan is an integral part of the vertebrate intestinal microbiome. How protozoan integrates into a commensal bacteria-enriched ecosystem remains poorly studied. Here, using a murine commensal Tritrichomonas musculis as a proof-of-concept, we studied potential factors involved in shaping the intestinal protozoan-bacteria community. Understanding the rules by which microbes form a multispecies community is crucial to prevent or correct microbial community dysfunctions to promote the host's health or to treat diseases.

我们目前对肠道中宿主-菌群相互作用的理解主要是针对原核细菌群落的研究。但是，存在一个未被重视的共生真核生物多样性社区，它是哺乳动物微生物群的组成部分。共生的原生动物细菌如何相互作用形成一个稳定的微生物群落仍然知之甚少。在这里，我们描述了一种在物种上被系统地命名为Tritrichomonas musculis的鼠类动物共生体，其在肠道中的定殖导致野生型C57BL / 6小鼠的肠道细菌丰度和多样性降低。同时，饮食中的营养和共生细菌也影响了原生动物肠道的定殖和稳定性。用正常食物饮食的小鼠体内有丰富的T. musculis，转而使用西式高脂饮食会导致肠道动物原生动物的数量减少。在高脂饮食中补充菊粉作为膳食纤维可部分恢复原生动物的定殖。另外，即使在高脂低纤维饮食条件下，广谱抗生素混合物也允许了穆氏弧菌的植入。此外，口服双歧杆菌属。加上高脂饮食中菊粉的饮食补充，以双歧杆菌物种依赖性方式影响了原生动物的肠道植入。总的来说，我们的研究描述了饮食依赖养分的鼠共生原生动物-细菌串扰作为宿主肠道微生物组重要调节剂的一个例子。

重要性：与共生细菌一样，共生原生动物是脊椎动物肠道微生物组的组成部分。原生动物如何整合到富含共生细菌的生态系统中的研究仍很少。在这里，我们以鼠科Tritrichomonas musculis作为概念证明，研究了影响肠道原生动物细菌群落形成的潜在因素。了解微生物形成多物种群落的规则对于预防或纠正微生物群落功能障碍以促进宿主的健康或治疗疾病至关重要。