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Characterization of myocardial lesions associated with cardiomyopathy syndrome in A tlantic salmon, S almo salar L ., using laser capture microdissection
Author(s) -
WiikNielsen J,
Løvoll M,
Fritsvold C,
Kristoffersen A B,
Haugland Ø,
Hordvik I,
Aamelfot M,
Jirillo E,
Koppang E O,
Grove S
Publication year - 2012
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/j.1365-2761.2012.01431.x
Subject(s) - laser capture microdissection , biology , endocardium , pathology , microdissection , population , myocarditis , cardiomyopathy , immunohistochemistry , microbiology and biotechnology , pathogenesis , myocyte , immunology , heart failure , gene expression , medicine , biochemistry , environmental health , gene
Cardiomyopathy syndrome ( CMS ) in Atlantic salmon, S almo salar L ., is characterized by focal infiltration in the spongy myocardium and endocardium of the heart. The origin of the mononuclear infiltrate is unknown. Using experimentally infected fish, we investigated localization of the causative agent, piscine myocarditis virus ( PMCV ), within the heart and characterized the cell population associated with myocardial lesions. Cellular and transcriptional characteristics in the lesions were compared with adjacent non‐infiltrated tissues using laser capture microdissection, RT ‐q PCR and immunohistochemistry. Our results reveal that PMCV is almost exclusively present in myocardial lesions. The inflammatory infiltrate comprises a variety of leucocyte populations, including T cells, B cells, MHC class II + and CD 83 + cells, most likely of the macrophage line. Correlation analyses demonstrated co‐ordinated leucocyte activity at the site of the virus infection. Cellular proliferation and/or DNA repair was demonstrated within the myocardial lesions. Different cell populations, mainly myocytes, stained positive for proliferating cell nuclear antigen ( PCNA ). Densities of endothelial cells and fibroblasts were not significantly increased. The simultaneous presence of PMCV and various inflammatory cells in all myocardial lesions analysed may indicate that both viral lytic and immunopathological effects may contribute to the pathogenesis of CMS .