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Open AccessArticle

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

1
Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
2
Department of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
3
Center of Infectious Disease and Signaling Research, National Cheng Kung University, Tainan 701, Taiwan
*
Author to whom correspondence should be addressed.
Viruses 2018, 10(12), 690; https://doi.org/10.3390/v10120690
Received: 18 October 2018 / Revised: 24 November 2018 / Accepted: 28 November 2018 / Published: 5 December 2018
(This article belongs to the Special Issue Cytoskeleton in Virus Infections)
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. View Full-Text
Keywords: dengue virus; microglia; migration; caveolae; MIP-3β dengue virus; microglia; migration; caveolae; MIP-3β
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MDPI and ACS Style

Jhan, M.-K.; Shen, T.-J.; Tseng, P.-C.; Wang, Y.-T.; Lin, C.-F. Signaling of Macrophage Inflammatory Protein (MIP)-3β Facilitates Dengue Virus-Induced Microglial Cell Migration. Viruses 2018, 10, 690.

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