Open AccessToll-Like Receptor Stimulation Enhances Phagocytosis and Intracellular Killing of Nonencapsulated and EncapsulatedStreptococcus pneumoniaeby Murine Microglia
Author(s) -
Sandra Ribes,
Sandra Ebert,
Tommy Regen,
Amit Agarwal,
Simone C. Tauber,
Dirk Czesnik,
Annette Spreer,
Stephanie Bunkowski,
Helmut Eiffert,
Uwe Hanisch,
Sven Hammerschmidt,
Roland Nau
Publication year - 2010
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.01110-09
Subject(s) - microglia , tlr2 , biology , phagocytosis , streptococcus pneumoniae , microbiology and biotechnology , tlr4 , innate immune system , lipopolysaccharide , toll like receptor , lipoteichoic acid , stimulation , receptor , immunology , inflammation , immune system , bacteria , biochemistry , antibiotics , genetics , neuroscience , staphylococcus aureus
Toll-like receptors (TLRs) are crucial pattern recognition receptors in innate immunity that are expressed in microglia, the resident macrophages of the brain. TLR2, -4, and -9 are important in the responses againstStreptococcus pneumoniae , the most common agent causing bacterial meningitis beyond the neonatal period. Murine microglial cultures were stimulated with agonists for TLR1/2 (Pam3 CSK4 ), TLR4 (lipopolysaccharide), and TLR9 (CpG oligodeoxynucleotide) for 24 h and then exposed to either the encapsulated D39 (serotype 2) or the nonencapsulated R6 strain ofS. pneumoniae . After stimulation, the levels of interleukin-6 and CCL5 (RANTES [regulated upon activation normal T-cell expressed and secreted]) were increased, confirming microglial activation. The TLR1/2, -4, and -9 agonist-stimulated microglia ingested significantly more bacteria than unstimulated cells (P 90% of phagocytosis. Along with an increased phagocytic activity, the intracellular bacterial killing was also increased in TLR-stimulated cells compared to unstimulated cells. Together, our data suggest that microglial stimulation by these TLRs may increase the resistance of the brain against pneumococcal infections.