PUBLICATION

Effect of ES-products from Anisakis (Nematoda: Anisakidae) on experimentally induced colitis in adult zebrafish

Authors
Haarder, S., Kania, P.W., Holm, T.L., von Gersdorff Jørgensen, L., Buchmann, K.
ID
ZDB-PUB-170806-1
Date
2017
Source
Parasite immunology   39(10): (Journal)
Registered Authors
Keywords
Anisakis, IBD, qPCR, Colitis, helminth therapy, zebrafish
MeSH Terms
  • Animals
  • Anisakis/immunology*
  • Anisakis/metabolism*
  • Colitis/chemically induced
  • Colitis/drug therapy*
  • Cytokines/metabolism
  • Fish Diseases/drug therapy*
  • Gene Expression
  • Helminth Proteins/pharmacology*
  • Humans
  • Intestines/pathology
  • Larva/immunology
  • Larva/metabolism
  • Male
  • Mice
  • Zebrafish
PubMed
28779539 Full text @ Parasite Immunol.
Abstract
Inflammatory bowel disease (IBD) in developed countries is linked with elevated hygienic standards. One of several factors involved in this question may be reduced exposure to the immunomodulatory effects of parasitic helminths. Several investigations on treatment of mice and humans with helminth-derived substances have supported this notion, but underlying mechanisms remain unclear. The present study therefore dissects to what extent a series of immune-related genes are modulated in zebrafish with experimentally induced colitis following exposure to excretory-secretory (ES) products isolated from larval Anisakis, a widely distributed fish nematode. Adult zebrafish intrarectally exposed to the colitis-inducing agent TNBS developed severe colitis leading to 80% severe morbidity but if co-injected (i.p.) with Anisakis ES-products the morbidity rate was 50% at the end of the experiment (48 hours post exposure). Gene expression studies of TNBS treated zebrafish showed clear upregulation of a range of genes encoding inflammatory cytokines and effector molecules and some induction of genes related to the adaptive response. A distinct innate-driven immune response was seen in both TNBS and TNBS+ES group, but expression values were significantly depressed for several important pro-inflammatory genes in the TNBS+ES group, indicating protective mechanisms of Anisakis ES compounds on intestinal immunopathology in zebrafish. This article is protected by copyright. All rights reserved.
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Expression
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Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping