کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2431449 1106759 2014 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Evidence of immune and inflammatory processes in the gills of AGD-affected Atlantic salmon, Salmo salar L.
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک علوم آبزیان
پیش نمایش صفحه اول مقاله
Evidence of immune and inflammatory processes in the gills of AGD-affected Atlantic salmon, Salmo salar L.
چکیده انگلیسی


• 2D quantitative RT-PCR was used to map the transcriptional responses in AGD-affected gills of Atlantic salmon.
• Neoparamoeba perurans elicits a classical inflammatory response in the gills of AGD-affected A. salmon.
• Expression of immune genes within gill lesions misrepresents the cellular immune response in the gills during AGD.
• AGD elicited an increased expression of cellular markers, most notably antigen presenting cells, B-cells and T-cells.
• T-cells within the AGD-affected gills are mainly constituted of CD8+ cells and not CD4+ T-cells.

Amoebic gill disease (AGD) is a disease caused by the ectoparasite Neoparamoeba perurans which affects several cultured marine fish worldwide. The characterisation of pro-inflammatory and immune related genes at the mRNA level in AGD-affected Atlantic salmon gills was performed at 10 days post-inoculation using 2D quantitative RT-PCR, a method of mapping transcriptional responses in tissues. The genes of interest were IL-1β, TNF-α, TCR-α chain, CD8, CD4, MHC-IIα, MHC-I, IgM and IgT. A significant increase in expression of the mRNA of all the genes was observed in the gills of AGD-affected fish. Contrary to previous studies, our data suggest that the parasite, N. perurans, elicits a classical inflammatory response in the gills of AGD-affected fish and indicates that the mRNA expression of immune genes within gill lesions misrepresents the cellular immune response in the gills during AGD.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Fish & Shellfish Immunology - Volume 36, Issue 2, February 2014, Pages 563–570
نویسندگان
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