Toll-Like Receptor Stimulation Enhances Phagocytosis and Intracellular Killing of Nonencapsulated and Encapsulated Streptococcus pneumoniae by Murine Microglia
2010 | journal article. A publication with affiliation to the University of Göttingen.
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Toll-Like Receptor Stimulation Enhances Phagocytosis and Intracellular Killing of Nonencapsulated and Encapsulated Streptococcus pneumoniae by Murine Microglia
Ribes, S.; Ebert, S.; Regen, T.; Agarwal, A.; Tauber, S. C.; Czesnik, D. & Spreer, A. et al. (2010)
Infection and Immunity, 78(2) pp. 865-871. DOI: https://doi.org/10.1128/IAI.01110-09
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Details
- Authors
- Ribes, Sandra; Ebert, Sandra; Regen, Tommy; Agarwal, Amit; Tauber, Simone C.; Czesnik, Dirk; Spreer, Annette; Bunkowski, Stephanie; Eiffert, Helmut; Hanisch, Uwe-Karsten; Hammerschmidt, Sven; Nau, Roland
- Abstract
- 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 against Streptococcus pneumoniae, the most common agent causing bacterial meningitis beyond the neonatal period. Murine microglial cultures were stimulated with agonists for TLR1/2 (Pam3CSK4), TLR4 (lipopolysaccharide), and TLR9 (CpG oligodeoxynucleotide) for 24 h and then exposed to either the encapsulated D39 (serotype 2) or the nonencapsulated R6 strain of S. 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 < 0.05). The presence of cytochalasin D, an inhibitor of actin polymerizaton, blocked >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.
- Issue Date
- 2010
- Status
- published
- Publisher
- Amer Soc Microbiology
- Journal
- Infection and Immunity
- ISSN
- 0019-9567