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* Department of Neurology, Klinikum Grosshadern, and
Max von Pettenkofer-Institute for Hygiene and Microbiology, Ludwig-Maximilians University, Munich, Germany; and
Institute of Medical Microbiology, Immunology, and Hygiene, Technical University of Munich, Munich, Germany
Heterologous expression of Toll-like receptor (TLR)2 and CD14 in
Chinese hamster ovary fibroblasts was reported to confer responsiveness
to pneumococcal peptidoglycan. The present study characterized the role
of TLR2 in the host immune response and clinical course of pneumococcal
meningitis. Pneumococcal infection of mice caused a significant
increase in brain TLR2 mRNA expression at both 4 and 24 h
postchallenge. Mice with a targeted disruption of the
TLR2 gene (TLR2-/-) showed a
moderate increase in disease severity, as evidenced by an aggravation
of meningitis-induced intracranial complications, a more pronounced
reduction in body weight and temperature, and a deterioration of motor
impairment. These symptoms were associated with significantly higher
cerebellar and blood bacterial titers. Brain expression of the
complement inhibitor complement receptor-related protein y was
significantly higher in infected TLR2-/- than in
wild-type mice, while the expression of the meningitis-relevant
inflammatory mediators IL-1
, TNF-
, IL-6, macrophage-inflammatory
protein (MIP)-2, inducible NO synthase, and C3 was similar in both
genotypes. We first ectopically expressed single candidate receptors in
HEK293 cells and then applied peritoneal macrophages from mice lacking
TLR2 and/or functional TLR4 for further analysis. Overexpression
of TLR2 and TLR4/MD-2 conferred activation of NF-
B in response to
pneumococcal exposure. However, pneumococci-induced TNF- release
from peritoneal macrophages of wild-type and TLR2/functional
TLR4/double-deficient mice did not differ. Thus, while TLR2 plays a
significant role in vivo, yet undefined pattern recognition receptors
contribute to the recognition of and initiation of the host immune
defense toward Streptococcus pneumoniae
infection.
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D. Torres, M. Barrier, F. Bihl, V. J. F. Quesniaux, I. Maillet, S. Akira, B. Ryffel, and F. Erard Toll-Like Receptor 2 Is Required for Optimal Control of Listeria monocytogenes Infection Infect. Immun., April 1, 2004; 72(4): 2131 - 2139. [Abstract] [Full Text] [PDF]
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M. G. Netea, R. Sutmuller, C. Hermann, C. A. A. Van der Graaf, J. W. M. Van der Meer, J. H. van Krieken, T. Hartung, G. Adema, and B. J. Kullberg Toll-Like Receptor 2 Suppresses Immunity against Candida albicans through Induction of IL-10 and Regulatory T Cells J. Immunol., March 15, 2004; 172(6): 3712 - 3718. [Abstract] [Full Text] [PDF]
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S. Knapp, C. W. Wieland, C. van 't Veer, O. Takeuchi, S. Akira, S. Florquin, and T. van der Poll Toll-Like Receptor 2 Plays a Role in the Early Inflammatory Response to Murine Pneumococcal Pneumonia but Does Not Contribute to Antibacterial Defense J. Immunol., March 1, 2004; 172(5): 3132 - 3138. [Abstract] [Full Text] [PDF]
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J. Branger, S. Knapp, S. Weijer, J. C. Leemans, J. M. Pater, P. Speelman, S. Florquin, and T. van der Poll Role of Toll-Like Receptor 4 in Gram-Positive and Gram-Negative Pneumonia in Mice Infect. Immun., February 1, 2004; 72(2): 788 - 794. [Abstract] [Full Text] [PDF]
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S. H. Han, J. H. Kim, M. Martin, S. M. Michalek, and M. H. Nahm Pneumococcal Lipoteichoic Acid (LTA) Is Not as Potent as Staphylococcal LTA in Stimulating Toll-Like Receptor 2 Infect. Immun., October 1, 2003; 71(10): 5541 - 5548. [Abstract] [Full Text] [PDF]
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