Publication details

Evaluation of Microbiome-Host Relationships in the Zebrafish Gastrointestinal System Reveals Adaptive Immunity Is a Target of Bis(2-ethylhexyl) Phthalate (DEHP) Exposure

Authors

ADAMOVSKÝ Ondřej BUERGER Amanda N. VESPALCOVÁ Hana SOHAG Shahadur R. HANLON Amy T. GINN Pamela E. CRAFT Serena L. SMATANA Stanislav BUDINSKÁ Eva PERSICO Maria BISESI Joseph H., Jr. MARTYNIUK Christopher J.

Year of publication 2020
Type Article in Periodical
Magazine / Source Environmental Science & Technology
MU Faculty or unit

Faculty of Science

Citation
Web https://pubs.acs.org/doi/10.1021/acs.est.0c00628
Doi http://dx.doi.org/10.1021/acs.est.0c00628
Keywords DI(2-ETHYLHEXYL) PHTHALATE; AIRWAY INFLAMMATION; INTESTINAL FAILURE; ENTEROCYTE MASS; TIGHT JUNCTIONS; CELLS; NEUROPEPTIDES; ASSOCIATIONS; CITRULLINE; EXPRESSION
Attached files
Description To improve physical characteristics of plastics such as flexibility and durability, producers enrich materials with phthalates such as di-2-(ethylhexyl) phthalate (DEHP). DEHP is a high production volume chemical associated with metabolic and immune disruption in animals and humans. To reveal mechanisms implicated in phthalate-related disruption in the gastrointestinal system, male and female zebrafish were fed DEHP (3 ppm) daily for two months. At the transcriptome level, DEHP significantly upregulated gene networks in the intestine associated with helper T cells' (Th1, Th2, and Th17) specific pathways. The activation of gene networks associated with adaptive immunity was linked to the suppression of networks for tight junction, gap junctional intercellular communication, and transmembrane transporters, all of which are precursors for impaired gut integrity and performance. On a class level, DEHP exposure increased Bacteroidia and Gammaproteobacteria and decreased Verrucomicrobiae in both the male and female gastrointestinal system. Further, in males there was a relative increase in Fusobacteriia and Betaproteobacteria and a relative decrease in Saccharibacteria. Predictive algorithms revealed that the functional shift in the microbiome community, and the metabolites they produce, act to modulate intestinal adaptive immunity. This finding suggests that the gut microbiota may contribute to the adverse effects of DEHP on the host by altering metabolites sensed by both intestinal and immune Th cells. Our results suggest that the microbiome-gut-immune axis can be modified by DEHP and emphasize the value of multiomics approaches to study microbiome-host interactions following chemical perturbations.
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