Billy Vincent, Lhotská Zuzana, Jirků Milan, Kadlecová Oldřiška, Frgelecová Lucia, Parfrey Laura Wegener, Pomajbíková Kateřina Jirků
Department of Zoology, Biodiversity Research Centre, University of British Columbia, Vancouver, BC, Canada.
Institute of Parasitology, Biology Centre, Czech Academy of Sciences, České Budějovice, Czechia.
Front Microbiol. 2021 Apr 7;12:641483. doi: 10.3389/fmicb.2021.641483. eCollection 2021.
Protists are a normal component of mammalian intestinal ecosystems that live alongside, and interact with, bacterial microbiota. , one of the most common intestinal eukaryotes, is reported as a pathogen that causes inflammation and disease, though health consequences likely vary depending on host health, the gut ecosystem, and genetic diversity. Accumulating evidence suggests that is by and large commensal. is more common in healthy individuals than those with immune mediated diseases such as Inflammatory Bowel Diseases (IBD). presence is also associated with altered composition and higher richness of the bacterial gut microbiota. It is not clear whether directly promotes a healthy gut and microbiome or is more likely to colonize and persist in a healthy gut environment. We test this hypothesis by measuring the effect of ST3 colonization on the health and microbiota in a rat experimental model of intestinal inflammation using the haptenizing agent dinitrobenzene sulfonic acid (DNBS). We experimentally colonized rats with ST3 obtained from a healthy, asymptomatic human donor and then induced colitis after 3 weeks (short term exposure experiment) or after 13 weeks (long term exposure experiment) and compared these colonized rats to a colitis-only control group. Across experiments ST3 colonization alters microbiome composition, but not richness, and induces only mild gut inflammation but no clinical symptoms. Our results showed no effect of short-term exposure to ST3 on gut inflammation following colitis induction. In contrast, long-term exposure appears to promote a faster recovery from colitis. There was a significant reduction in inflammatory markers, pathology 2 days after colitis induction in the colonized group, and clinical scores also improved in this group. colonization resulted in a significant reduction in tumor necrosis factor alpha (TNFα) and IL-1β relative gene expression, while expression of IFNγ and IL17re/17C were elevated. We obtained similar results in a previous pilot study. We further found that bacterial richness rebounded in rats colonized by ST3. These results suggest that sp. may alter the gut ecosystem in a protective manner and promote faster recovery from disturbance.
原生生物是哺乳动物肠道生态系统的正常组成部分,与细菌微生物群共同生活并相互作用。尽管健康后果可能因宿主健康状况、肠道生态系统和遗传多样性而异,但作为最常见的肠道真核生物之一,被报道为一种会引发炎症和疾病的病原体。越来越多的证据表明,大体上是共生的。在健康个体中比在患有免疫介导疾病(如炎症性肠病,IBD)的个体中更常见。的存在还与肠道细菌微生物群的组成改变和丰富度增加有关。目前尚不清楚它是直接促进肠道和微生物群的健康,还是更有可能在健康的肠道环境中定殖并持续存在。我们通过使用半抗原化剂二硝基苯磺酸(DNBS),在大鼠肠道炎症实验模型中测量ST3定殖对健康和微生物群的影响,来检验这一假设。我们用从一名健康、无症状的人类供体获得的ST3对大鼠进行实验性定殖,然后在3周后(短期暴露实验)或13周后(长期暴露实验)诱导结肠炎,并将这些定殖大鼠与仅患结肠炎的对照组进行比较。在各个实验中,ST3定殖会改变微生物群组成,但不会改变丰富度,并且仅诱导轻度肠道炎症但无临床症状。我们的结果表明,短期暴露于ST3对诱导结肠炎后的肠道炎症没有影响。相比之下,长期暴露似乎能促进结肠炎更快恢复。在定殖组中,结肠炎诱导后2天炎症标志物、病理学显著降低,该组的临床评分也有所改善。定殖导致肿瘤坏死因子α(TNFα)和IL-1β相对基因表达显著降低,而IFNγ和IL17re/17C的表达升高。我们在之前的一项初步研究中也得到了类似的结果。我们进一步发现,被ST3定殖的大鼠中细菌丰富度出现反弹。这些结果表明,sp.可能以一种保护性方式改变肠道生态系统,并促进从干扰中更快恢复。