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

Research output: Contribution to journalArticle

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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.

Original languageEnglish
Article number274025
JournalMediators of Inflammation
Volume2015
DOIs
Publication statusPublished - 2015 Jan 1

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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

Cite this

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. In: Mediators of Inflammation. 2015 ; Vol. 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.

In: Mediators of Inflammation, Vol. 2015, 274025, 01.01.2015.

Research output: Contribution to journalArticle

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