ZFIN ID: ZDB-PUB-050714-7
Effects of Arsenic on Zebrafish Innate Immune System
Hermann, A.C., and Kim, C.H.
Date: 2005
Source: Marine biotechnology (New York, N.Y.)   7(5): 494-505 (Journal)
Registered Authors: Kim, Carol H.
Keywords: arsenic, respiratory burst, zebrafish, interferon, Mx, TNF-alpha
MeSH Terms:
  • Animals
  • Arsenic/antagonists & inhibitors
  • Arsenic/toxicity*
  • DNA Primers
  • DNA Virus Infections/metabolism
  • Fish Diseases/immunology
  • Gene Expression/drug effects
  • Immunity, Innate/drug effects*
  • Immunocompetence/drug effects
  • Interferons/biosynthesis
  • Interferons/genetics
  • Larva/metabolism
  • Novirhabdovirus/immunology
  • Polymerase Chain Reaction/methods
  • RNA, Messenger/biosynthesis
  • RNA, Messenger/drug effects
  • Respiratory Burst/drug effects*
  • Rhabdoviridae Infections/immunology
  • Rhabdoviridae Infections/veterinary
  • Tumor Necrosis Factor-alpha/biosynthesis
  • Tumor Necrosis Factor-alpha/genetics
  • Zebrafish/immunology*
  • Zebrafish/metabolism*
  • Zebrafish/virology
PubMed: 16007375 Full text @ Mar. Biotechnol.
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ABSTRACT
The innate immune response, the first line of defense against invading pathogens, can be perturbed by environmental toxicants such as arsenic. This study reports the effects of arsenic on innate immunity of zebrafish. Respiratory burst activity, messenger RNA expression of tumor necrosis factor alpha (TNF-alpha), a primer of the respiratory burst response, and mRNA expression of the antiviral cytokines interferon (IFN) and MX, before and after viral infection, were examined in arsenic-exposed zebrafish larvae. Respiratory burst activity and TNF-alpha expression were decreased upon arsenic exposure, indicating inhibition of TNF-alpha priming of the respiratory burst response. Arsenic enhanced IFN expression slightly over time, but reduced MX expression. In zebrafish infected with snakehead rhabdovirus, arsenic decreased induction and altered the kinetics of IFN and MX upon infection. Differences in IFN and MX expression in arsenic-exposed larvae point toward an interruption of the Janus kinase-signal transducer and activator of transcription (JAK/STAT) pathway.
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