Signaling of Macrophage Inflammatory Protein (MIP)-3β Facilitates Dengue Virus-Induced Microglial Cell Migration

Ming-Kai Jhan, Ting-Jing Shen, Po-Chun Tseng, Yung-Ting Wang, Chiou-Feng Lin

Research output: Contribution to journalArticlepeer-review

Abstract

The infection by dengue virus (DENV) of microglia causes cell activation and migration via a mechanism involving viral entry, RNA release, and Toll-like receptor 3 signaling. In this study, we demonstrated that secreted chemotactic factors present in microglial conditioned medium (MCM) facilitated cell motility in the murine BV2 microglial cells. The pharmacological disruption of lipid rafts/caveolae reduced DENV-and ultraviolet (UV)-inactivated MCM-induced microglial cell migration. An antibody-based cytokine/chemokine array showed an increase in macrophage inflammatory protein (MIP)-3β in MCM produced using DENV-infected cells. The pharmacological inhibition of c-Jun N-terminal kinase (JNK) retarded UV-MCM-induced microglial cell migration. These results demonstrate that secreted MIP-3β and its effect on the JNK signaling pathways mediates DENV-induced BV2 microglial cell migration.

Original languageEnglish
JournalViruses
Volume10
Issue number12
DOIs
Publication statusPublished - Dec 1 2018

Keywords

  • Caveolae
  • Dengue virus
  • MIP-3β
  • Microglia
  • Migration

ASJC Scopus subject areas

  • Infectious Diseases
  • Virology

Fingerprint Dive into the research topics of 'Signaling of Macrophage Inflammatory Protein (MIP)-3β Facilitates Dengue Virus-Induced Microglial Cell Migration'. Together they form a unique fingerprint.

Cite this