Increased level of IL-32 during human immunodeficiency virus infection suppresses HIV replication
- 作者：Sahibzada T. Rasool ; Heng Tang ; Jianmei Wu ; Wei Li ; Muhammad Mahmood Mukhtar ; Jingwen Zhang ; Yongxin Mu ; Huang Xioa Xing ; Jianguo Wu ; Ying Zhu
- 关键词：Interleukin-32 ; HIV ; siRNA
- 刊名：Immunology Letters
- 出版年：2008
- 期刊代码：115_01652478
- 类别：med
- 出版时间：15 May 2008
- 卷：117
- 期：2
- 页码：161-167
- 文件大小：392 K
摘要
Interleukin-32 was recently identified as a pro-inflammatory cytokine produced by T-lymphocytes, natural killer cells, epithelial cells, and blood monocytes. IL-32 is induced by IFN-γ in a time-dependent manner suggesting a role for IL-32 in innate and adaptive immune responses. In this study we present evidence that Human immunodeficiency virus promotes interleukin-32 production at both mRNA and protein levels. Our results showed that there is a 74%increase in the serum levels of IL-32 among HIV patients as compared to healthy individuals. There was a three-fold increase in the promoter activity of the IL-32 in the present infections HIV clone. This increase in IL-32 promoter activity was substantiated by increased IL-32 mRNA and protein levels. We have also demonstrated that IL-32 suppresses HIV replication. Our results show that HIV LTR activity was increased by more than six-folds when endogenous IL-32 was knocked down by IL-32-specific siRNA whereas it decreased by one-fold when IL-32 was over expressed in the cells. Similarly a more than two-fold increase and a 50%decrease in HIV p24 values were noted when IL-32 was knocked down and when IL-32 was over expressed in the cells, respectively. Our present work shows that raised IL-32 levels in HIV infection may in turn hamper HIV replication; one of the protective mechanisms of nature.