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Pathological changes in the immune organs of broiler chickens fed on corn naturally contaminated with aflatoxins B1 and B2
Authors:Xi Peng  Shiping Bai  Xuemei Ding  Qiufeng Zeng  Jing Fang
Affiliation:1. Institute of Animal Nutrition, Key Laboratory for Animal Disease-Resistance Nutrition of China Ministry of Education, Sichuan Agricultural University, Yaan, Sichuan, People's Republic of China;2. College of Veterinary Medicine, Sichuan Agricultural University, Yaan, Sichuan, People's Republic of China;3. College of Veterinary Medicine, Sichuan Agricultural University, Yaan, Sichuan, People's Republic of China
Abstract:The purpose of this study was to evaluate the underlying basis for aflatoxin-induced immunosuppression in the broiler chicken by detecting pathological lesions and apoptosis in thymus, bursa of Fabricius (BF) and spleen. COBB500? male broiler chicks were randomly allocated to two groups. The control group was fed on a basal corn-based diet while the other group (the AFB group) was fed on a similar diet but the corn was naturally contaminated with aflatoxins B1 and B2. Histopathological examination revealed that in the AFB group there was more nuclear debris in the three immune organs and obvious congestion of red pulp in the spleen, when compared with the control group. Ultrastructural examination showed lesions in the lymphocytes and reticulocytes of the three immune organs, the mucosal epithelium of the BF and the plasmocytes of the spleen. Increased apoptotic cells and an impaired membrane system (including nuclear membrane, mitochondria and endoplasmic reticulum [ER]) could be observed in the three immune organs in birds of the AFB group. In the plasmocytes, dilated rough endoplasmic reticulum contained electron-dense matrix. By flow cytometry, the percentages of apoptosis were significantly higher (P < 0.01) in the three organs of the AFB group than those of the control group. These observations suggested that the lesions of the immune organs were related to the immunosuppression, and that the apoptosis might be initiated by the mitochondrial pathway and ER chaperone pathway.
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