ena-STUDY-UNIVERSITY OF BRITISH COLUMBIA-28-01-2021-21:42:29:378-357
Effect of Blastocystis ST3 on the rat gut microbiota before and after DNBS-induced colitis
Protists are a normal component of mammalian intestinal ecosystems that live alongside, andinteract with, bacterial microbiota. Blastocystis, one of the most common intestinaleukaryotes, is reported as a pathogen that causes inflammation and disease, though healthconsequences likely vary depending on host health, the gut ecosystem, and genetic diversity.Accumulating evidence suggests that Blastocystis is by and large commensal. Blastocystis ismore common in healthy individuals than those with immune mediated diseases such asInflammatory Bowel Diseases (IBD). Blastocystis presence is also associated with alteredcomposition and higher richness of the bacterial gut microbiota. It is not clear whetherBlastocystis directly promotes a healthy gut and microbiome or is more likely to colonize andpersist in a healthy gut environment. We test this hypothesis by measuring the effect ofBlastocystis ST3 colonization on the health and microbiota in a rat experimental model ofintestinal 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 three weeks (short term exposureexperiment) or after 13 weeks (long term exposure experiment) and compared thesecolonized rats to a colitis-only control group. Across experiments Blastocystis ST3colonization alters microbiome composition, but not richness, and induces only mild gutinflammation but no clinical symptoms. Our results showed no effect of short-term exposureto Blastocystis ST3 on gut inflammation following colitis induction. In contrast, long-termBlastocystis exposure appears to promote a faster recovery from colitis. There was asignificant reduction in inflammatory markers, pathology two days after colitis induction inthe colonized group, and clinical scores also improved in this group. Blastocystis colonizationresulted in a significant reduction in tumor necrosis factor alpha (TNFa) and IL-1b relativegene expression, while expression of IFNa and 17re/IL17C were elevated. We obtainedsimilar results in a previous pilot study. We further found that bacterial richness rebounded inrats 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.
Protists are a normal component of mammalian intestinal ecosystems that live alongside, andinteract with, bacterial microbiota. Blastocystis, one of the most common intestinaleukaryotes, is reported as a pathogen that causes inflammation and disease, though healthconsequences likely vary depending on host health, the gut ecosystem, and genetic diversity.Accumulating evidence suggests that Blastocystis is by and large commensal. Blastocystis ismore common in healthy individuals than those with immune mediated diseases such asInflammatory Bowel Diseases (IBD). Blastocystis presence is also associated with alteredcomposition and higher richness of the bacterial gut microbiota. It is not clear whetherBlastocystis directly promotes a healthy gut and microbiome or is more likely to colonize andpersist in a healthy gut environment. We test this hypothesis by measuring the effect ofBlastocystis ST3 colonization on the health and microbiota in a rat experimental model ofintestinal 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 three weeks (short term exposureexperiment) or after 13 weeks (long term exposure experiment) and compared thesecolonized rats to a colitis-only control group. Across experiments Blastocystis ST3colonization alters microbiome composition, but not richness, and induces only mild gutinflammation but no clinical symptoms. Our results showed no effect of short-term exposureto Blastocystis ST3 on gut inflammation following colitis induction. In contrast, long-termBlastocystis exposure appears to promote a faster recovery from colitis. There was asignificant reduction in inflammatory markers, pathology two days after colitis induction inthe colonized group, and clinical scores also improved in this group. Blastocystis colonizationresulted in a significant reduction in tumor necrosis factor alpha (TNFa) and IL-1b relativegene expression, while expression of IFNa and 17re/IL17C were elevated. We obtainedsimilar results in a previous pilot study. We further found that bacterial richness rebounded inrats 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.