Acquired protective immune response in a fish-myxozoan model encompasses specific antibodies and inflammation resolution

The myxozoan parasite Enteromyxum leei causes chronic enteritis in gilthead sea bream (GSB, Sparus aurata) leading to intestinal dysfunction. Two trials were performed in which GSB that had survived a previous infection with E. leei (SUR), and naïve GSB (NAI), were exposed to water effluent containi...

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Published inFish & shellfish immunology Vol. 90; pp. 349 - 362
Main Authors Picard-Sánchez, Amparo, Estensoro, Itziar, del Pozo, Raquel, Piazzon, M. Carla, Palenzuela, Oswaldo, Sitjà-Bobadilla, Ariadna
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.07.2019
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Summary:The myxozoan parasite Enteromyxum leei causes chronic enteritis in gilthead sea bream (GSB, Sparus aurata) leading to intestinal dysfunction. Two trials were performed in which GSB that had survived a previous infection with E. leei (SUR), and naïve GSB (NAI), were exposed to water effluent containing parasite stages. Humoral factors (total IgM and IgT, specific anti-E. leei IgM, total serum peroxidases), histopathology and gene expression were analysed. Results showed that SUR maintained high levels of specific anti-E. leei IgM (up to 16 months), expressed high levels of immunoglobulins at the intestinal mucosa, particularly the soluble forms, and were resistant to re-infection. Their acquired-type response was complemented by other immune effectors locally and systemically, like cell cytotoxicity (high granzyme A expression), complement activity (high c3 and fucolectin expression), and serum peroxidases. In contrast to NAI, SUR displayed a post-inflammatory phenotype in the intestine and head kidney, characteristic of inflammation resolution (low il1β, high il10 and low hsp90α expression). [Display omitted] •Resistance to E. leei in re-exposed fish lasts up to 16 months.•Specific antibodies (IgM) have a protective role for re-exposed fish at early times.•Re-exposed fish show inflammatory resolution phenotype in intestine and head kidney.•Cell cytotoxicity, peroxidases, and complement contribute to acquired resistance.
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ISSN:1050-4648
1095-9947
DOI:10.1016/j.fsi.2019.04.300