Dengue Virus Infection Causes the Activation of Distinct NF- κ B Pathways for Inducible Nitric Oxide Synthase and TNF- Expression in RAW264.7 Cells

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

研究成果: Article

6 引文 (Scopus)

摘要

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

原文English
文章編號274025
期刊Mediators of Inflammation
2015
DOIs
出版狀態Published - 2015 一月 1

指紋

Dengue Virus
Nitric Oxide Synthase Type II
Virus Diseases
Nitric Oxide
Viral Proteins
Transcription Factors
Hot Temperature
Macrophages
Pharmacology
Infection

All Science Journal Classification (ASJC) codes

  • Immunology
  • Cell Biology

引用此文

Cheng, Yi Lin ; Lin, Yee Shin ; Chen, Chia Ling ; Wan, Shu Wen ; Ou, Yi Dan ; Yu, Chia Yi ; Tsai, Tsung Ting ; Tseng, Po Chun ; Lin, Chiou Feng. / Dengue Virus Infection Causes the Activation of Distinct NF- κ B Pathways for Inducible Nitric Oxide Synthase and TNF- Expression in RAW264.7 Cells. 於: Mediators of Inflammation. 2015 ; 卷 2015.
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abstract = "Infection with dengue virus (DENV) causes an increase in proinflammatory responses, such as nitric oxide (NO) generation and TNF-expression; however, the molecular mechanism underlying this inflammatory activation remains undefined, although the activation of the transcription factor NF-B is generally involved. In addition to TNF- production in DENV-infected murine macrophage RAW264.7 cells, inducible NO synthase was transcriptionally and posttranslationally elevated and accompanied by NO generation. NF-B is known to be activated by DENV infection. Pharmacologically inhibiting NF-B activation abolishes iNOS/NO biosynthesis and TNF- production. With inhibition, the potential role of NF-B 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-B activation; however, it effectively abolished inducible iNOS/NO biosynthesis but did not inhibit TNF- production. In contrast to TLR3, viral protein NS2B3 also independently contributed to NF-B activation to regulate TNF- production. These results show the distinct pathways for NF-B activation caused by DENV infection individually for the regulation of iNOS/NO and TNF- expression.",
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Dengue Virus Infection Causes the Activation of Distinct NF- κ B Pathways for Inducible Nitric Oxide Synthase and TNF- Expression in RAW264.7 Cells. / Cheng, Yi Lin; Lin, Yee Shin; Chen, Chia Ling; Wan, Shu Wen; Ou, Yi Dan; Yu, Chia Yi; Tsai, Tsung Ting; Tseng, Po Chun; Lin, Chiou Feng.

於: Mediators of Inflammation, 卷 2015, 274025, 01.01.2015.

研究成果: Article

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AU - Lin, Yee Shin

AU - Chen, Chia Ling

AU - Wan, Shu Wen

AU - Ou, Yi Dan

AU - Yu, Chia Yi

AU - Tsai, Tsung Ting

AU - Tseng, Po Chun

AU - Lin, Chiou Feng

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N2 - Infection with dengue virus (DENV) causes an increase in proinflammatory responses, such as nitric oxide (NO) generation and TNF-expression; however, the molecular mechanism underlying this inflammatory activation remains undefined, although the activation of the transcription factor NF-B is generally involved. In addition to TNF- production in DENV-infected murine macrophage RAW264.7 cells, inducible NO synthase was transcriptionally and posttranslationally elevated and accompanied by NO generation. NF-B is known to be activated by DENV infection. Pharmacologically inhibiting NF-B activation abolishes iNOS/NO biosynthesis and TNF- production. With inhibition, the potential role of NF-B 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-B activation; however, it effectively abolished inducible iNOS/NO biosynthesis but did not inhibit TNF- production. In contrast to TLR3, viral protein NS2B3 also independently contributed to NF-B activation to regulate TNF- production. These results show the distinct pathways for NF-B activation caused by DENV infection individually for the regulation of iNOS/NO and TNF- expression.

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