Blastocystis Colonization Alters the Gut Microbiome and, in Some Cases, Promotes Faster Recovery From Induced Colitis.
Blastocystis Colonization Alters the Gut Microbiome and, in Some Cases, Promotes Faster Recovery From Induced Colitis.
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DOI：
10.3389/fmicb.2021.641483
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发表时间：
2021
影响因子：
5.2
通讯作者：
Pomajbíková KJ
中科院分区：
文献类型：
--
作者：
Billy V;Lhotská Z;Jirků M;Kadlecová O;Frgelecová L;Parfrey LW;Pomajbíková KJ
原生生物是哺乳动物肠道生态系统的正常组成部分，与细菌微生物群一起生活并相互作用。芽囊原虫是最常见的肠道真核生物之一，据报道是一种引起炎症和疾病的病原体，尽管健康后果可能因宿主健康、肠道生态系统和遗传多样性而异。越来越多的证据表明，芽囊原虫基本上是寄生性的。囊胚在健康个体中比那些患有免疫介导的疾病如炎症性肠病（IBD）的人更常见。芽囊原虫的存在也与细菌肠道微生物群的组成改变和更高的丰富度有关。目前尚不清楚囊胚是否直接促进健康的肠道和微生物组，或者更有可能在健康的肠道环境中定植和持续存在。我们通过使用半抗原化剂二硝基苯磺酸（DNBS）测量囊胚ST 3定殖对肠道炎症大鼠实验模型中的健康和微生物群的影响来测试这一假设。我们用从健康、无症状的人类供体中获得的芽囊原虫ST 3对大鼠进行实验性定植，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，并将这些定植的大鼠与结肠炎进行比较仅对照组。在所有实验中，芽囊原虫ST 3定植改变了微生物组的组成，但没有丰富性，并且仅诱导轻度肠道炎症，但没有临床症状。我们的研究结果表明，短期暴露于囊胚ST 3对结肠炎诱导后的肠道炎症没有影响。相比之下，长期接触囊胚似乎可以促进结肠炎的更快恢复。在结肠炎诱导后2天，定植组的炎症标志物和病理学显著减少，该组的临床评分也有所改善。囊胚定植导致肿瘤坏死因子α（TNFα）和IL-1β相关基因表达显著降低，而IFNγ和IL 17 re/17 C表达升高。我们在以前的试点研究中获得了类似的结果。我们进一步发现，细菌丰富度反弹，在大鼠由囊胚ST 3殖民。这些结果表明，芽囊原虫可能会以保护性的方式改变肠道生态系统，并促进更快地从干扰中恢复。
Protists are a normal component of mammalian intestinal ecosystems that live alongside, and interact with, bacterial microbiota. Blastocystis, 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 Blastocystis is by and large commensal. Blastocystis is more common in healthy individuals than those with immune mediated diseases such as Inflammatory Bowel Diseases (IBD). Blastocystis presence is also associated with altered composition and higher richness of the bacterial gut microbiota. It is not clear whether Blastocystis 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 Blastocystis 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 Blastocystis 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 Blastocystis 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 Blastocystis ST3 on gut inflammation following colitis induction. In contrast, long-term Blastocystis 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. Blastocystis 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 Blastocystis ST3. These results suggest that Blastocystis sp. may alter the gut ecosystem in a protective manner and promote faster recovery from disturbance.
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影响因子：
3.6
作者：
Krogsgaard LR;Andersen LO';Johannesen TB;Engsbro AL;Stensvold CR;Nielsen HV;Bytzer P
通讯作者：
Bytzer P
影响因子：
48
作者：
Callahan BJ;McMurdie PJ;Rosen MJ;Han AW;Johnson AJ;Holmes SP
通讯作者：
Holmes SP
影响因子：
6.4
作者：
Comeau AM;Douglas GM;Langille MG
通讯作者：
Langille MG
影响因子：
4.1
作者：
Hirano, Atsushi;Umeno, Junji;Esaki, Motohiro
通讯作者：
Esaki, Motohiro
影响因子：
2
作者：
Chandramathi, S.;Suresh, Kumar Govind;Kuppusamy, U. R.
通讯作者：
Kuppusamy, U. R.