Publisert 2023

Les på engelsk


Tidsskrift : Aquaculture , vol. 572 , p. 1–12–0 , 2023

Utgiver : Elsevier

Internasjonale standardnummer :
Trykt : 0044-8486
Elektronisk : 1873-5622

Publikasjonstype : Vitenskapelig artikkel

Bidragsytere : Karlsen, Christian Renè; Ytteborg, Elisabeth; Furevik, Anette; Sveen, Lene; Tunheim, Siv Haugen; Afanasyev, Sergey; Tingbø, Monica Gausdal; Krasnov, Aleksei


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Kjetil Aune


Skin is the first line of defence against waterborne pathogens, such as Moritella viscosa, which is the causative agent of winter ulcer disease in Atlantic salmon (Salmo salar L.). The present study revealed that vaccination protects against both M. viscosa-induced mortality and skin ulceration, but protection varied according to the strain used in the vaccine formulation. Examination of skin tissue 4 days post M. viscosa challenge indicated that M. viscosa initiated infection by colonising the scale surface. Sequencing the transcripts of the variable region of the IgM heavy chain did not detect effect of vaccination or M. viscosa challenge on antibody repertoire and B cell trafficking from the lymphatic organs to skin. Skin layer-specific responses were examined with 44 K oligonucleotide microarray. Skin responded to vaccination and M. viscosa challenge by increasing transcription of structural genes, stimulating metabolism, and regulation of developmental processes. Immune responses to dead (vaccine) and live M. viscosa were very similar and no pathogen-specific changes were found. Combined use of skin transcriptional profiles and image analysis revealed differences in the infected skin layers between the study groups. M. viscosa was likely retained in the epidermis of vaccinated salmon, whereas the dermis was colonised in unvaccinated fish. Furthermore, decreased expression of lymphocyte-specific and antiviral genes in the dermis indicated possible evasion of immune-related cells from skin in salmon challenged with M. viscosa. Our data also indicated that intraperitoneal vaccination may prime the humoral innate response, which enables a rapid response in the dermis layer of skin during M. viscosa invasion.


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