Effects of cyanobacterial toxin microcystin-LR on the transcription levels of immune-related genes in grass carp Ctenopharyngodon idella

被引:0
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作者
Lili Wei
Baojian Sun
MingXian Chang
Yi Liu
Pin Nie
机构
[1] Chinese Academy of Sciences,State Key Laboratory of Freshwater Ecology and Biotechnology, and Laboratory of Fish Diseases, Institute of Hydrobiology
[2] Jiangxi Agricultural University,College of Animal Science and Technology
来源
Environmental Biology of Fishes | 2009年 / 85卷
关键词
Grass carp; Immune-relate genes; Microcystin-LR; Immunotoxicity; Quantitative real-time PCR;
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学科分类号
摘要
Recent studies in mammals have revealed that the cyanobacterial toxin MC-LR suppresses immune functions. Nevertheless, immunotoxic effects of microcystins have been little studied in fish. In this paper, we present the profiles of the immune modulation of MC-LR in grass carp, and quantitative real-time PCR methodology was developed for the measurement of relative transcription changes of six immune-related genes in the spleen and head kidney of the grass carp Ctenopharyngodon idella, which were intraperitoneally injected with 50 μg MC-LR·kg-1 body weight in a three-week period. This study was focused exclusively on gene transcription level changes at different time points after MC-LR exposure, so, only one dose was given. The investigated genes were interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), type I interferon (Type I IFN), peptidoglycan recognition protein-L (PGRP-L), immunoglobulin M (IgM) and major histocompatibility complex class I (MHC-I) genes. The results demonstrated that the transcription levels of the TNF-α, type I IFN, and PGRP-L genes in the spleen and head kidney were significantly low at all time points, and those of IL-1β were significantly low in the head kidney at different time points. In addition, IgM and MHC-I transcription levels were only significantly low in the spleen and head kidney at 21 d postinjection. The changes in the transcription levels of immune-related genes induced by MC-LR confirmed its effect on inhibiting immune function at the transcription level.
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