C57BL/6 and A/J Mice Have Different Inflammatory Response and Liver Lipid Profile in Experimental Alcoholic Liver Disease

被引:14
作者
Bavia, Lorena [1 ,2 ]
de Castro, Iris Arantes [1 ]
Isaac, Lourdes [1 ]
机构
[1] Univ Sao Paulo, Inst Ciencias Biomed, Dept Imunol, BR-05508900 Sao Paulo, SP, Brazil
[2] Fundacao Oswaldo Cruz, Inst Carlos Chagas, BR-81350010 Curitiba, Parana, Brazil
基金
巴西圣保罗研究基金会;
关键词
TUMOR-NECROSIS-FACTOR; HIGH-FAT DIET; INSULIN-RESISTANCE; FACTOR-ALPHA; METABOLIC SYNDROME; IMMUNE-RESPONSES; ANIMAL-MODELS; ETHANOL; PATHOGENESIS; COMPLEMENT;
D O I
10.1155/2015/491641
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Alcoholic liver disease (ALD) is an important worldwide public health issue characterized by liver steatosis, inflammation, necrosis, and apoptosis of hepatocytes with eventual development of fibrosis and cirrhosis. Comparison of murine models with different inflammatory responses for ALD is important for an evaluation of the importance of genetic background in the interpretation of ethanol-induced phenotypes. Here, we investigated the role of inflammation and genetic background for the establishment of ALD using two different mouse strains: C57BL/6 (B6) and A/J. B6 and A/J mice were treated with a high fat diet containing ethanol (HFDE) and compared to the controls for 10 weeks. Hepatomegaly and steatohepatitis were similar in B6 and A/J mice, but only A/J mice were resistant to weight gain. On the other hand, HFDE-fed B6 accumulated more triglycerides (TG) and cholesterol and presented more intense cellular infiltrate in the liver when compared to HFDM-fed mice. Liver inflammatory environment was distinct in these two mouse strains. While HFDE-fed B6 produced more liver IL-12, A/J mice increased the TNF-alpha production. We concluded that mouse genetic background could dictate the intensity of the HFDE-induced liver injury.
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页数:11
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