ArticleMarine biotechnology (New York, N.Y.)2010
EseD, a putative T3SS translocon component of Edwardsiella tarda, contributes to virulence in fish and is a candidate for vaccine development.
Article in Marine biotechnology (New York, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 28 citations in OpenAlex.
- Toxin Secretion Systems Used by Marine Pathogenic Bacteria: A Review.Journal of fish diseases · 2026Review
- Field Prevalence and Pathological Features ofAnimals : an open access journal from MDPI · 2025Article
- Functional analysis of ascP in Aeromonas veronii TH0426 reveals a key role in the regulation of virulence.Journal of microbiology (Seoul, Korea) · 2022Article
- The Involvement of Thiamine Uptake in the Virulence ofPathogens (Basel, Switzerland) · 2022Article
- A peek into mass mortality caused by antimicrobial resistantBiologia · 2022Article
- Construction and evaluation of type III secretion system mutants of the catfish pathogen Edwardsiella piscicida.Journal of fish diseases · 2018Article
- Article
- Type III Secretion System Translocon Component EseB Forms Filaments on and Mediates Autoaggregation of and Biofilm Formation by Edwardsiella tarda.Applied and environmental microbiology · 2015Article
- Aeromonas salmonicida subsp. salmonicida in the light of its type-three secretion system.Microbial biotechnology · 2014Review
- Pathogenesis of and strategies for preventing Edwardsiella tarda infection in fish.Veterinary research · 2012Review
- Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Edwardsiella tarda has a type III secretion system (T3SS) essential for pathogenesis. EseD, together with EseB and EseC, has been suggested to form a putative T3SS translocon complex, although its further function is unclear. To investigate the physiological role of EseD, a mutant strain of E. tarda was constructed with an in-frame deletion of the entire eseD gene. One finding was that the ∆eseD mutant decreased the secretion levels of EseC and EseB proteins. Additionally, the ∆eseD mutant showed attenuated swarming and contact-hemolysis abilities. However, the ∆eseD mutant showed increased biofilm formation. Complementation of the mutant strain with eseD restored these phenotypes to those similar to the wild-type strain. Furthermore, infection experiments in fish showed that the ∆eseD mutant exhibited slower proliferation and a tenfold decrease in virulence in fish. These results indicate a specific role of EseD in the pathogenesis of E. tarda. Finally, recombinant EseD protein elicited high antibody titers in immunized fish and various levels of protection against lethal challenge with the wild-type strain. These results indicate that EseD protein may be a candidate antigen for development of a subunit vaccine against Edwardsiellosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.