Dengue Virus Infection Causes the Activation of Distinct NF-κB Pathways for Inducible Nitric Oxide Synthase and TNF-α Expression in RAW264.7 CellsReportar como inadecuado




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Mediators of Inflammation - Volume 2015 2015, Article ID 274025, 13 pages -

Research Article

Institute of Basic Medical Science, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan

Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan

Center of Infectious Diseases and Signaling Research, National Cheng Kung University, Tainan 701, Taiwan

Translational Research Center, Taipei Medical University, Taipei 110, Taiwan

Department of Microbiology and Immunology, College of Medicine, Taipei Medical University, Taipei 110, Taiwan

Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan

Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan

Received 29 October 2014; Revised 14 April 2015; Accepted 19 May 2015

Academic Editor: Dennis D. Taub

Copyright © 2015 Yi-Lin Cheng et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Infection with dengue virus DENV causes an increase in proinflammatory responses, such as nitric oxide NO generation and TNF-α expression; however, the molecular mechanism underlying this inflammatory activation remains undefined, although the activation of the transcription factor NF-κB is generally involved. In addition to TNF-α production in DENV-infected murine macrophage RAW264.7 cells, inducible NO synthase was transcriptionally and posttranslationally elevated and accompanied by NO generation. NF-κB is known to be activated by DENV infection. Pharmacologically inhibiting NF-κB activation abolishes iNOS-NO biosynthesis and TNF-α production. With inhibition, the potential role of NF-κB in oxidative signaling regulation was prevented during DENV infection. Heat-inactivated DENV failed to cause the identified inflammatory responses. Pharmacological inhibition of TLR3 partly decreased NF-κB activation; however, it effectively abolished inducible iNOS-NO biosynthesis but did not inhibit TNF-α production. In contrast to TLR3, viral protein NS2B3 also independently contributed to NF-κB activation to regulate TNF-α production. These results show the distinct pathways for NF-κB activation caused by DENV infection individually for the regulation of iNOS-NO and TNF-α expression.





Autor: Yi-Lin Cheng, Yee-Shin Lin, Chia-Ling Chen, Shu-Wen Wan, Yi-Dan Ou, Chia-Yi Yu, Tsung-Ting Tsai, Po-Chun Tseng, and Chiou-

Fuente: https://www.hindawi.com/



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