4.5 Article

Expression of AIM2 is correlated with increased inflammation in chronic hepatitis B patients

期刊

VIROLOGY JOURNAL
卷 12, 期 -, 页码 -

出版社

BIOMED CENTRAL LTD
DOI: 10.1186/s12985-015-0360-y

关键词

-

类别

资金

  1. Science and Technology of Shandong, China [2011GSF12111]
  2. Nature Science Foundation of Shandong Province [2014ZRB14315]

向作者/读者索取更多资源

Background: The absent in melanoma 2 (AIM2), a cytosolic dsDNA inflammasome, can be activated by viral DNA to trigger caspase-1. Its role in immunopathology of chronic hepatitis B and C virus (HBV, HCV) infection is still largely unclear. In this study, the expression AIM2, and its downstream cytokines, caspase-1, IL-18 and IL-1 beta, in liver tissue of patients with chronic hepatitis B and C (CHB, CHC) were investigated. Methods: A total of 70 patients diagnosed with chronic hepatitis were enrolled, including 47 patients with CHB and 23 patients with CHC. A liver biopsy was taken from each patient, and immunohistochemistry was used to detect the expression of AIM2 and inflammatory factors caspase-1, IL-18, and IL-1 beta in the biopsy specimens. The relationship between AIM2 expression and these inflammatory factors was analyzed. Results: The expression of AIM2 in CHB patients (89.4 %) was significantly higher than in CHC patients (8.7 %), and among the CHB patients, the expression of AIM2 was significantly higher in the high HBV replication group (HBV DNA >= 1 x 10(5) copies/mL) than in the low HBV replication group (HBV DNA < 1 x 10(5) copies/mL). The expression of AIM2 was also correlated with HBV-associated inflammatory activity in CHB patients statistically. Additionally, AIM2 levels were positively correlated with the expression of caspase-1, IL-1 beta and IL-18 in CHB patients, which implied that the AIM2 expression is directly correlated with the inflammatory activity associated with CHB. Conclusions: AIM2 upregulation may be a component of HBV immunopathology. The underlying mechanism and possible signal pathway warrant further study.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.5
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据