Blastocystis Colonization Alters the Gut Microbiome and, in Some Cases, Promotes Faster Recovery From Induced Colitis

Abstract

Protists are a normal component of mammalian intestinal ecosystems that live alongside, and interact with, bacterial microbiota. <i>Blastocystis</i>, 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 <i>Blastocystis</i> is by and large commensal. <i>Blastocystis</i> is more common in healthy individuals than those with immune mediated diseases such as Inflammatory Bowel Diseases (IBD). <i>Blastocystis</i> presence is also associated with altered composition and higher richness of the bacterial gut microbiota. It is not clear whether <i>Blastocystis</i> 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 <i>Blastocystis</i> 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 <i>Blastocystis</i> 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 <i>Blastocystis</i> 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 <i>Blastocystis</i> ST3 on gut inflammation following colitis induction. In contrast, long-term <i>Blastocystis</i> 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. <i>Blastocystis</i> 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 <i>Blastocystis</i> ST3. These results suggest that <i>Blastocystis</i> sp. may alter the gut ecosystem in a protective manner and promote faster recovery from disturbance.