ArticleFrontiers in cellular and infection microbiology2016
Edwardsiella tarda-Induced Inhibition of Apoptosis: A Strategy for Intracellular Survival.
Article in Frontiers in cellular and infection microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 55 citations in OpenAlex.
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- Mycoplasma glycine cleavage system key subunit GcvH is an apoptosis inhibitor targeting host endoplasmic reticulum.PLoS pathogens · 2024Article
- An intracellular bacterial pathogen triggers RIG-I/MDA5-dependent necroptosis.Current research in microbial sciences · 2024Article
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- Immune Response and Apoptosis-Related Pathways Induced byPathogens (Basel, Switzerland) · 2021Article
- Tauroursodeoxycholic acid prevents Burkholderia pseudomallei-induced endoplasmic reticulum stress and is protective during melioidosis in mice.BMC microbiology · 2021Article
- The Zebrafish Antiapoptotic Protein BIRC2 PromotesFrontiers in immunology · 2021Article
- Transcriptome Analysis ofInternational journal of molecular sciences · 2020Article
- RNA-Sequencing Analyses of Small Bacterial RNAs and their Emergence as Virulence Factors in Host-Pathogen Interactions.International journal of molecular sciences · 2020Review
- A Comparative Analysis ofInternational journal of molecular sciences · 2019Article
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- Intracellular Trafficking Pathways ofFrontiers in cellular and infection microbiology · 2017Article
- Neutrophil Extracellular Traps ofFrontiers in immunology · 2017Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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