Document Detail


Interleukin-6 expression was regulated by epigenetic mechanisms in response to influenza virus infection or dsRNA treatment.
MedLine Citation:
PMID:  21353307     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Interleukin-6 (IL-6) is a multifunctional cytokine that plays critical roles in a wide range of biologic activities. However, it remains unknown whether epigenetic mechanisms are involved in these processes. The possible epigenetic mechanisms involved in IL-6 expression during influenza virus (IV) infection were investigated in this study. Our results showed that both IV and its replicative intermediate dsRNA activated the IL-6 promoter, increased its transcription and enhanced cytokine secretion. IL-6 was up-regulated by DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (DAC) treatment, while its promoter activity was decreased when promoter DNA was methylated in vitro. Further study found that the IL-6 proximal promoter region was demethylated after both IV infection and dsRNA treatment, subsequently impairing its binding by transcription factors. Moreover, the DNA methyltransferase (DNMT) activity was inhibited in dsRNA treated nuclei, and DNMT1 but not DNMT3a or DNMT3b was responsible for IL-6 expression in this process. These results implied that IL-6 expression was regulated by promoter demethylation induced by down-regulation of DNMT activity. Our work revealed that epigenetic mechanisms regulate host genes expression in IV infection, and provided a new insight into understanding the mechanisms of viral infection.
Authors:
Bikui Tang; Ruihua Zhao; Yong Sun; Ying Zhu; Jiang Zhong; Guoping Zhao; Naishuo Zhu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-02-24
Journal Detail:
Title:  Molecular immunology     Volume:  48     ISSN:  1872-9142     ISO Abbreviation:  Mol. Immunol.     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-03-14     Completed Date:  2011-06-10     Revised Date:  2013-06-03    
Medline Journal Info:
Nlm Unique ID:  7905289     Medline TA:  Mol Immunol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1001-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Ltd. All rights reserved.
Affiliation:
Department of Microbiology and Microbial Engineering, School of Life Sciences, State Key Laboratory of Genetic Engineering, Institute of Biomedical Sciences, Fudan University, Shanghai 200433, PR China.
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MeSH Terms
Descriptor/Qualifier:
Azacitidine / analogs & derivatives,  pharmacology
Base Sequence
Binding Sites / genetics
Cell Line, Tumor
CpG Islands / genetics
DNA (Cytosine-5-)-Methyltransferase / genetics,  metabolism
DNA Methylation / drug effects
Electrophoretic Mobility Shift Assay
Enzyme Inhibitors / pharmacology
Epigenesis, Genetic*
Gene Expression
HEK293 Cells
Host-Pathogen Interactions
Humans
Influenza A Virus, H5N1 Subtype / physiology*
Interleukin-6 / genetics*,  metabolism
Molecular Sequence Data
Promoter Regions, Genetic / genetics
Protein Binding / drug effects
RNA Interference
RNA, Double-Stranded / genetics*
Transcription Factors / metabolism
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Interleukin-6; 0/RNA, Double-Stranded; 0/Transcription Factors; 320-67-2/Azacitidine; 776B62CQ27/decitabine; EC 2.1.1.37/DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37/DNA (cytosine-5-)-methyltransferase 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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