Dengue virus infection increases microglial cell migration.
Ming-Kai JhanTsung-Ting TsaiChia-Ling ChenCheng-Chieh TsaiYi-Lin ChengYi-Chao LeeChiung-Yuan KoYee-Shin LinChih-Peng ChangLiang-Tzung LinChiou-Feng LinPublished in: Scientific reports (2017)
Activated microglial cells are present in dengue virus (DENV)-infected brains; however, the possible effects of DENV on microglia remain unclear. Here, we demonstrated DENV caused infection, including viral entry, RNA replication, viral protein expression, and virus release, in the murine microglial cell line BV2. DENV infection caused an increase in the formation of the multipolar phenotype in vitro and in vivo without affecting cell growth and cytotoxicity. DENV infection considerably increased cell motility and disrupting either actin filaments or clathrin retarded such effect. Increase in cell migration was only occurred by DENV infection following a clathrin-regulated endocytosis of DENV entry. Ultraviolet-inactivated DENV did not affect cell migration, and pharmacologically blocking toll-like receptor (TLR) 3 and TLR3-related signaling pathways reduced the DENV-induced increase in cell migration. These results demonstrate an advanced effect of DENV infection on microglial migration via a mechanism involving viral entry, RNA release, and TLR3 signal activation.
Keyphrases
- dengue virus
- cell migration
- zika virus
- toll like receptor
- inflammatory response
- aedes aegypti
- lipopolysaccharide induced
- lps induced
- immune response
- neuropathic pain
- nuclear factor
- induced apoptosis
- signaling pathway
- bone marrow
- oxidative stress
- pseudomonas aeruginosa
- single cell
- spinal cord injury
- mesenchymal stem cells
- escherichia coli
- cystic fibrosis
- cell proliferation
- staphylococcus aureus