Department of Hematology, LaBIOMED, Torrance, 90502, CA 90502, USA.
Exp Mol Pathol. 2012 Apr;92(2):191-3. doi: 10.1016/j.yexmp.2012.01.001. Epub 2012 Jan 16.
Mallory-Denk body (MDB) formation is a component of alcoholic and non alcoholic hepatitis. Proteins of the TLR pathway were shown to be involved in the formation of MDBs, in mice fed DDC. TLR genes are upregulated and SAMe supplementation prevents this up regulation and prevented the formation of MDBs. DNA of livers from control mice, from mice fed DDC 10weeks, refed 1week with DDC and with DDC+SAMe were extracted and used to study the methylation pattern of genes involves in the TLR pathway. A PCR array was used to analyze it. Using PCR arrays for the mouse TLR pathway,24 genes were found whose expression of IL12A was regulated by the methylation of its gene. DDC fed for 10weeks reduced the methylation of the IL12A gene expression. This expression was also reduced when DDC was refed. However, when SAMe was fed, the intermediate level methylation of IL12A was up regulated to the intermediate level and the methylation of the promoter decreased compared to DDC refeeding or DDC 10weeks. IL12A is known to induce the production of IFNg by NK and L(T). We showed in a previous publication that IFNg is one of the major cytokines involved in the induction of MDB formation. The low expression of IL12A associated with the intermediate methylation of its promoter could explain one step in the mechanism which leads to the formation of MDBs.
Mallory-Denk 小体 (MDB) 的形成是酒精性和非酒精性肝炎的一个组成部分。研究表明,TLR 途径的蛋白参与了 DDC 喂养小鼠 MDB 的形成。TLR 基因上调,SAMe 补充可防止这种上调,并防止 MDB 的形成。从对照组小鼠、10 周喂养 DDC 的小鼠、1 周复喂 DDC 的小鼠和用 DDC+SAMe 喂养的小鼠的肝脏中提取 DNA,并用于研究参与 TLR 途径的基因的甲基化模式。使用 PCR 阵列进行分析。使用用于小鼠 TLR 途径的 PCR 阵列,发现有 24 个基因的 IL12A 表达受其基因甲基化的调节。10 周喂养 DDC 降低了 IL12A 基因表达的甲基化。当 DDC 复喂时,这种表达也会降低。然而,当给予 SAMe 时,IL12A 的中间水平甲基化被上调到中间水平,与 DDC 复喂或 DDC 10 周相比,其启动子的甲基化减少。IL12A 已知可诱导 NK 和 L(T)产生 IFNg。我们在之前的一篇出版物中表明,IFNg 是参与诱导 MDB 形成的主要细胞因子之一。与 IL12A 启动子中间甲基化相关的低表达可能解释了导致 MDB 形成的机制中的一个步骤。