Transcriptomic analysis of the impacts of ethinylestradiol (EE2) and its consequences for proliferative kidney disease outcome in rainbow trout (Oncorhynchus mykiss).


Journal

Comparative biochemistry and physiology. Toxicology & pharmacology : CBP
ISSN: 1532-0456
Titre abrégé: Comp Biochem Physiol C Toxicol Pharmacol
Pays: United States
ID NLM: 100959500

Informations de publication

Date de publication:
Aug 2019
Historique:
received: 21 12 2018
revised: 19 03 2019
accepted: 13 04 2019
pubmed: 21 4 2019
medline: 2 7 2019
entrez: 21 4 2019
Statut: ppublish

Résumé

Freshwater fish are threatened by the cumulative impact of multiple stressors. The purpose of this study was to unravel the molecular and organism level reactions of rainbow trout, Oncorhynchus mykiss, to the combined impact of two such stressors that occur in the natural habitat of salmonids. Fish were infected with either the myxozoan parasite, Tetracapsuloides bryosalmonae, which causes proliferative kidney disease (PKD), or exposed to ethinylestradiol (EE2) an estrogenic endocrine disrupting compound, or to a combination of both (PKD × EE2). PKD is a slow progressive chronic disease here we focused on a later time point (130-day post-infection (d.p.i.)) when parasite intensity in the fish kidney has already started to decrease. At 130 d.p.i., RNA-seq technology was applied to the posterior kidney, the main target organ for parasite development. This resulted with 280 (PKD), 14 (EE2) and 444 (PKD × EE2) differentially expressed genes (DEGs) observed in the experimental groups. In fish exposed to the combination of stressors (PKD × EE2), a number of pathways were regulated that were neither observed in the single stressor groups. Parasite infection, alone and in combination with EE2, only resulted in a low intensity immune response that negatively correlated with an upregulation of genes involved in a variety of metabolic and inflammation resolution processes. This could indicate a trade-off whereby the host increases investment in recovery/resolution processes over immune responses at a later stage of disease. When PKD infection took place under simultaneous exposure to EE2 (PKD × EE2), parasite intensity decreased and pathological alterations in the posterior kidney were reduced in comparison to the PKD only condition. These findings suggest that EE2 modulated these response profiles in PKD infected fish, attenuating the disease impact on the fish.

Identifiants

pubmed: 31004835
pii: S1532-0456(18)30320-X
doi: 10.1016/j.cbpc.2019.04.009
pii:
doi:

Substances chimiques

Ethinyl Estradiol 423D2T571U

Types de publication

Clinical Trial, Veterinary Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

31-48

Informations de copyright

Crown Copyright © 2019. Published by Elsevier Inc. All rights reserved.

Auteurs

Christyn Bailey (C)

University of Bern, Vetsuisse Faculty, Centre for Fish and Wildlife Health, Länggassstrasse 122, CH-3012 Bern, Switzerland; Fish Immunology and Pathology Laboratory, Animal Health Research Center (CISA-INIA), Madrid, Spain. Electronic address: christyn.bailey@vetsuisse.unibe.ch.

Elena Wernicke von Siebenthal (EW)

University of Bern, Vetsuisse Faculty, Centre for Fish and Wildlife Health, Länggassstrasse 122, CH-3012 Bern, Switzerland.

Kristina Rehberger (K)

University of Bern, Vetsuisse Faculty, Centre for Fish and Wildlife Health, Länggassstrasse 122, CH-3012 Bern, Switzerland.

Helmut Segner (H)

University of Bern, Vetsuisse Faculty, Centre for Fish and Wildlife Health, Länggassstrasse 122, CH-3012 Bern, Switzerland.

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Classifications MeSH