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The immunotoxicity of decabromodiphenyl ether (BDE-209) on broiler chicks by transcriptome profiling analysis

脾脏 免疫系统 生物 超氧化物歧化酶 肿瘤坏死因子α 细胞因子 转录组 脾细胞 免疫学 谷胱甘肽过氧化物酶 十溴二苯醚 过氧化氢酶 男科
作者
Lin Cheng,Qinxiong Rao,Qicai Zhang,Wei Song,Shuhui Guan,Zhilin Jiang,Tian Wu,Zhihui Zhao,Weiguo Song
出处
期刊:Ecotoxicology and Environmental Safety [Elsevier BV]
卷期号:232: 113284-113284
标识
DOI:10.1016/j.ecoenv.2022.113284
摘要

Decabromodiphenyl ether (BDE-209) has drawn significant attention due to its suppression of immune functions in animals and even humans. In order to explore the mechanism through which BDE-209 affects the immune system, broiler chicks were fed a diet containing various concentrations of BDE-209 (0, 0.004, 0.04, 0.4, and 4 g/kg) for 42 days. Histopathological observations of immune organs found damaged and necrotic lymphocytes in the spleen and bursa, and losses of lymphoid cells in thymic gland. The activities of catalase, glutathione, glutathione peroxidase, and superoxide dismutase in both the spleen and serum were affected by BDE-209. Obvious bioaccumulation effect was found in spleen tissues (high to 1339 ± 181.9 μg/kg). Furthermore, transcriptome sequencing analyses of the spleen identified 424 upregulated and 301 downregulated DEGs, and the cytokine-cytokine receptor interaction signal pathway was most significantly enriched based on the Kyoto Encyclopedia of Genes and Genomes database. Quantitative real-time PCR affirmed the decreased expressions of interleukin IL18, IL18R1, IL18RAP, IL21, as well as interferon gamma IFNG and tumor necrosis factor superfamily members TNFSF8, indicating significant interference to immunomodulation function and possible disease progression in inflammatory effects resulting from BDE-209 exposure. The immunotoxicity of BDE-209 may cause the suppression of immune and physiological functions of spleen cells, leading to inflammation and apoptosis and ultimately spleen atrophy.
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