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Epidermal response of rainbow trout to I chthyobodo necator : immunohistochemical and gene expression studies indicate a T h1‐/ T h2‐like switch
Author(s) -
Chettri J K,
Kuhn J A,
Jaafar R M,
Kania P W,
Møller O S,
Buchmann K
Publication year - 2014
Publication title -
journal of fish diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.819
H-Index - 85
eISSN - 1365-2761
pISSN - 0140-7775
DOI - 10.1111/jfd.12169
Subject(s) - biology , immune system , immunohistochemistry , population , cathelicidin , immunology , rainbow trout , gene expression , innate immune system , gene , genetics , medicine , environmental health , fishery , fish <actinopterygii>
Infections with the parasitic flagellate I chthyobodo necator (Henneguy, 1883) cause severe skin and gill disease in rainbow trout O ncorhynchus mykiss (Walbaum, 1792) juveniles. The epidermal disturbances including hyperplasia and mucous cell exhaustion caused by parasitization are known, but no details on specific cellular and humoral reactions have been presented. By applying gene expression methods and immunohistochemical techniques, further details of immune processes in the affected skin can be presented. A population of I . necator was established in the laboratory and used to induce an experimental infection of juvenile rainbow trout. The course of infection was followed by sampling for parasite enumeration, immunohistochemistry ( IHC ) and quantitative PCR (q PCR ) on days 0, 5, 9 and 14 post‐infection. IHC showed a significant increase in the occurrence of I g M ‐positive cells in the skin of the infected fish, whereas I g T ‐positive cells were eliminated and the number of CD 8‐positive cells declined. q PCR studies supported the IHC findings showing a significant increase in I g M and a decrease in the CD 8 gene expression. In addition, genes encoding innate immune genes such as lysozyme, SAA and cathelicidin 2 were up‐regulated. Expression of cytokines ( IL ‐1β, IL ‐4/13A, IL ‐6, IL ‐8, IL ‐10), the cell marker CD 4 and the transcription factor GATA 3 showed a significant increase after infection. Cytokine profiling including up‐regulation of IL ‐4/13A and IL ‐10 genes and transcription factor GATA 3 connected to the proliferation of I g M producing lymphocytes suggests a partial shift towards a T h2 response associated with the I . necator infection.