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In this study, we sought to demonstrate how the dysbiosis in zebrafish (D.rerio) that’s observed with low levels of arsenic (50ppb) could be a physiological response, rather than a purely ecological consequence of arsenic’s direct toxicity to microbial symbionts. To probe this question, we applied 16S based metagenomics to observe arsenic’s effects on the fish media, where no physiological processes exist, as well as how immunosuppressive doses of dexamethasone treatment (50ug/ml) may reflect arsenic dysbiosis within the fish microbiome. Consistent with arsenic’s cytotoxic potential, arsenic reduced average number of 16S sequences across both fish and media samples- an effect was much weaker among fish samples. Fish media exposed to arsenic showed decreased microbial diversity as well as UniFrac distance scores between arsenic samples relative to our control group. In fish however, both arsenic and dexamethasone exposure resulted in increased alpha diversity and inter-sample UniFrac distances relative to the control. PICRUSt 16S functional inference data also revealed significant changes in the amount of LPS production and cell antigen related KEGG Orthologs relative to our control, suggesting altered innate immune function. Taken together, our data suggests that the dysbiosis to the zebrafish microbiome at 50ppb may, in part, be a physiological response.
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Von Reusner, Jonathan Michael, "Arsenic Dysbiosis to the Zebrafish Microbiome: An Ecological or Physiological Response?" (2016). Senior Projects Spring 2016. 98.
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