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Hepatitis B virus X protein increases the IL-1β-induced NF-kB activation via interaction with evolutionarily conserved signaling intermediate in Toll pathways (ECSIT)
CHEN Wannan 1 #,LIU Lingling 1,JIAO Boyan 1,LIN Wansong 1,LIN Xinjian 2,LIN Xu 1 *
1.Key Laboratory of Ministry of Education for Gastrointestinal Cancer, Key Laboratory of Fujian Province for Tumor Microbiology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou,350108
2.Depatment of Medicine and UC San Diego Moores Cancer Center, University of California-San Diego,California, USA
*Correspondence author
#Submitted by
Subject:
Funding: the Specialized Research Fund for the Doctoral Program of Higher Education of China （No.No. 20123518120003), the Program of Fujian Natural Science Foundation）
Opened online:25 August 2014
Accepted by: none
Citation: CHEN Wannan,LIU Lingling,JIAO Boyan.Hepatitis B virus X protein increases the IL-1β-induced NF-kB activation via interaction with evolutionarily conserved signaling intermediate in Toll pathways (ECSIT)[OL]. [25 August 2014] http://en.paper.edu.cn/en_releasepaper/content/4606851
 
 
Hepatitis B virus X protein (HBx) transactivates multiple transcription factors including nuclear factor-kappa B (NF-κB) that regulates inflammatory-related genes. However, the regulatory mechanism of HBx in NF-κB activation remains largely unknown. This study reports that HBx augments the interleukin-1β (IL-1β)-induced NF-κB activation and interleukin-10 (IL-10) expression via interaction with a Toll-like receptor (TLR) adapter protein, ECSIT (evolutionarily conserved signaling intermediate in Toll pathways). GST pull-down and co-immunoprecipitation analyses showed that HBx directly interacted with ECSIT. Deletion analysis of HBx in a CytoTrap two-hybrid system revealed that the interaction region of HBx for ECSIT was attributed to aa 51-80. Co-transfection of HBx and ECSIT in IL-1β-stimulated cells appeared to activate IKK and IκB signaling pathway as phosphorylation of both IKK α/β and IκBα was increased whereas knockdown of ECSIT or HBx△51-80 mutant attenuated the phosphorylation. As a consequence of IκBα degradation, NF-kB was activated as evidenced by increases in NF-κB transcriptional activity and the nuclear translocation of p65 and p50 that resulted in the induction of IL-10. In contrast, knockdown of ECSIT by siRNA or treatment with an NF-κB selective inhibitor (helenalin) abolished the NF-κB activation and IL-10 expression. We conclude that ECSIT appears to be a novel HBx-interacting signal molecule and their interaction is mechanistically important in IL-1β induction of NF-κB activation.
Keywords:Hepatitis B virus X protein; Interleukin-1/Toll-like receptor; Nuclear factor-κB; ECSIT; Interleukin-10
 
 
 

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