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ZFIN ID: ZDB-PUB-160730-2
Edwardsiella tarda-Induced Inhibition of Apoptosis: A Strategy for Intracellular Survival
Zhou, Z.J., Sun, L.
Date: 2016
Source: Frontiers in cellular and infection microbiology   6: 76 (Journal)
Registered Authors:
Keywords: Edwardsiella tarda, apoptosis, intracellular replication, invasion, zebrafish
Microarrays: GEO:GSE81773
MeSH Terms:
  • Animals
  • Antibodies
  • Apoptosis/physiology
  • Caspase 3/metabolism
  • Cell Line
  • Cytoplasm/microbiology
  • Cytoplasm/pathology
  • Down-Regulation
  • Edwardsiella tarda/genetics
  • Edwardsiella tarda/immunology
  • Edwardsiella tarda/physiology*
  • Enterobacteriaceae Infections/immunology
  • Enterobacteriaceae Infections/microbiology
  • Enterobacteriaceae Infections/veterinary*
  • Fish Diseases/immunology
  • Fish Diseases/microbiology*
  • Fish Diseases/pathology*
  • Fish Diseases/prevention & control
  • Gene Knockdown Techniques
  • Host-Pathogen Interactions
  • Rats
  • Transcriptome
  • Zebrafish/genetics
  • Zebrafish/immunology*
  • Zebrafish/microbiology
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/immunology
  • Zebrafish Proteins/metabolism
PubMed: 27471679 Full text @ Front Cell Infect Microbiol
ABSTRACT
Edwardsiella tarda is a Gram-negative bacterial pathogen that can infect a wide range of freshwater and marine fish. One salient feature of E. tarda is the ability to survive and replicate in various host cells. In this study, we observed that E. tarda replicated robustly in the zebrafish cell line ZF4, and that E. tarda-infected cells exhibited no detectable signs of apoptosis. Global transcriptome analysis and quantitative real-time RT-PCR revealed that E. tarda infection generally significantly downregulated pro-apoptotic genes and upregulated anti-apoptotic genes. To investigate the role of apoptosis in E. tarda infection, two upregulated anti-apoptotic genes (Fech and Prx3) and two downregulated pro-apoptotic genes (Brms1a and Ivns1a) were overexpressed in zebrafish. Subsequent infection study showed that Fech and Prx3 overexpression significantly promoted E. tarda dissemination in and colonization of fish tissues, while Brms1a and Ivns1a overexpression significantly reduced E. tarda dissemination and colonization. Consistently, when Fech and Prx3 were knocked down in zebrafish, E. tarda infection was significantly inhibited, whereas Brms1a and Ivns1a knockdown significantly enhanced E. tarda infection. These results indicate for the first time that E. tarda prevents apoptosis in teleost as a strategy for intracellular survival, and that some putative apoptotic genes of teleost function in the apoptosis pathway probably in a manner similar to that in mammalian systems.
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