کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2433472 1106834 2007 17 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Molecular cloning and expression analysis of tumour necrosis factor-α in amoebic gill disease (AGD)-affected Atlantic salmon (Salmo salar L.)
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک علوم آبزیان
پیش نمایش صفحه اول مقاله
Molecular cloning and expression analysis of tumour necrosis factor-α in amoebic gill disease (AGD)-affected Atlantic salmon (Salmo salar L.)
چکیده انگلیسی

Tumour necrosis factor-alpha (TNF-α) is a key mediator of inflammation during amoebiasis of humans and mice. Atlantic salmon (Salmo salar L.) are also susceptible to infection by amoebae (Neoparamoeba spp.), inflicting a condition known as amoebic gill disease (AGD). Here, the role of TNF-α in AGD-pathogenesis was examined. Two Atlantic salmon TNF-α transcripts designated TNF-α1 and TNF-α2 together with their respective genes were cloned and sequenced. TNF-α1 is 1379 bp and consists of a 738 bp open reading frame (ORF) translating into a predicted protein of 246 amino acids. TNF-α2 is 1412 bp containing an ORF and translated protein the same lengths as TNF-α1. An anti-rainbow trout TNF-α polyclonal antibody that bound recombinant Atlantic salmon TNF-α1 and TNF-α2 was used to detect constitutive and inducible expression of TNF-α in various tissues. The anti-TNF-α antibody bound to a TNF-like protein ≈60 kDa that was constitutively expressed in a number of tissues in healthy Atlantic salmon. However, this protein was not detected in lysates from mitogen-stimulated head kidney leucocytes, despite up-regulation of TNF-α mRNAs under the same conditions. During the early onset of AGD in Atlantic salmon, there were no demonstrable differences in the gill tissue expression of TNF-α1, TNF-α2 nor the interleukin-1 beta (IL-1β), inducible nitric oxide synthase (iNOS) and interferon gamma (IFN-γ) mRNAs compared to tissue from healthy fish. In Atlantic salmon with advanced AGD, IL-1β but not TNF-α1 or TNF-α2 mRNAs was up-regulated and was lesion-restricted. Given that Neoparamoeba spp. modulated both TNF-α2 and IL-1β in head kidney leucocytes in vitro, it appears that rather than being recalcitrant to Neoparamoeba spp.-mediated TNF-α expression, either the parasite can influence the cytokine response during infection, there is ineffective signalling for TNF-α expression, or there are too few cells at the site of infection with the capacity to produce TNF-α. These data support our previous observation that IL-1β mRNA expression is up-regulated in AGD-affected tissue and that TNF-α is not intrinsic in AGD-pathogenesis.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Fish & Shellfish Immunology - Volume 23, Issue 5, November 2007, Pages 1015–1031
نویسندگان
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