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Appears in Collections:Aquaculture Journal Articles
Peer Review Status: Refereed
Title: Early steps in the European eel (Anguilla anguilla)-Vibrio vulnificus interaction in the gills: role of the RtxA13 toxin
Author(s): Callol, Agnes
Pajuelo, David
Ebbesson, Lars
Teles, Mariana
MacKenzie, Simon
Amaro, Carmen
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Keywords: European eel
Vibrio vulnificus
Host-pathogen relationship
Immune response
Issue Date: Apr-2015
Date Deposited: 17-Jun-2016
Citation: Callol A, Pajuelo D, Ebbesson L, Teles M, MacKenzie S & Amaro C (2015) Early steps in the European eel (Anguilla anguilla)-Vibrio vulnificus interaction in the gills: role of the RtxA13 toxin. Fish and Shellfish Immunology, 43 (2), pp. 502-509.
Abstract: Vibrio vulnificus is an aquatic gram-negative bacterium that causes a systemic disease in eels called warm-water vibriosis. Natural disease occurs via water born infection; bacteria attach to the gills (the main portal of entry) and spread to the internal organs through the bloodstream, provoking host death by haemorrhagic septicaemia. V.vulnificus produces a toxin called RtxA13 that hypothetically interferes with the eel immune system facilitating bacterial invasion and subsequent death by septic shock. The aim of this work was to study the early steps of warm-water vibriosis by analysing the expression of three marker mRNA transcripts related to pathogen recognition (tlr2 and tlr5) and inflammation (il-8) in the gills of eels infected by immersion with either the pathogen or a mutant deficient in rtxA13. Results indicate a differential response that is linked to the rtx toxin in the expression levels of the three measured mRNA transcripts. The results suggest that eels are able to distinguish innocuous from harmful microorganisms by the local action of their toxins rather than by surface antigens. Finally, the cells that express these transcripts in the gills are migratory cells primarily located in the second lamellae that re-locate during infection suggesting the activation of a specific immune response to pathogen invasion in the gill.
DOI Link: 10.1016/j.fsi.2015.01.009
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