The viral TLR3 agonist poly(I:C) stimulates phagocytosis and intracellular killing of Escherichia coli by microglial cells.
Stimulation of murine primary microglia with Toll-like receptor (TLR) agonists enhances their ability to phagocytose and kill bacteria. Here we show that the viral TLR3 agonist poly(I:C) stimulates the release of cyto-/chemokines and nitric oxide by microglia. Poly(I:C) increases microglial phagocytosis and intracellular killing of Escherichia coli K1, a pathogenic encapsulated bacterial strain, after 30 and 90 min of co-incubation. Stimulation with a viral epitope may strengthen the resistance of the brain to bacterial infections in vivo. Our data encourage animal experiments with poly(I:C) derivatives to assess whether this approach can increase the resistance of the CNS against bacterial infections.
Ribes
Sandra
S
Institute of Neuropathology, University of Göttingen, Robert Koch Str. 40, D-37075 Göttingen, Germany. sribes@med.uni-goettingen.de
Adam
Nina
N
Ebert
Sandra
S
Regen
Tommy
T
Bunkowski
Stephanie
S
Hanisch
Uwe-Karsten
UK
Nau
Roland
R
D000818:Animals; D000998:Antiviral Agents / Q000276:immunology*; D004926:Escherichia coli / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D017628:Microglia / Q000276:immunology* / Q000382:microbiology; D010587:Phagocytosis / Q000276:immunology*; D011070:Poly I-C / Q000276:immunology*; D051196:Toll-Like Receptor 3 / Q000276:immunology*
D000998:Antiviral Agents; C519703:TLR3 protein, mouse; D051196:Toll-Like Receptor 3; D011070:Poly I-C