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The Journal of Immunology, 2004, 172: 3132-3138.
Copyright © 2004 by The American Association of Immunologists

Toll-Like Receptor 2 Plays a Role in the Early Inflammatory Response to Murine Pneumococcal Pneumonia but Does Not Contribute to Antibacterial Defense1

Sylvia Knapp2,*, Catharina W. Wieland*, Cornelis van ’t Veer§, Osamu Takeuchi, Shizuo Akira, Sandrine Florquin{dagger} and Tom van der Poll*,{ddagger}

* Laboratory of Experimental Internal Medicine, Departments of {dagger} Pathology and {ddagger} Infectious Diseases, Tropical Medicine and AIDS, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; § Nutrition and Toxicology Research Institute, Department of General Surgery, University of Maastricht, Maastricht, The Netherlands; and Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan

Toll-like receptors (TLR) are crucial pattern recognition receptors in innate immunity. The importance of TLR2 in host defense against Gram-positive bacteria has been suggested by the fact that this receptor recognizes major Gram-positive cell wall components, such as peptidoglycan and lipoteichoic acid. To determine the role of TLR2 in pulmonary Gram-positive infection, we first established that TLR2 is indispensable for alveolar macrophage responsiveness toward Streptococcus pneumoniae. Nonetheless, TLR2 gene-deficient mice intranasally inoculated with S. pneumoniae at doses varying from nonlethal (with complete clearance of the infection) to lethal displayed only a modestly reduced inflammatory response in their lungs and an unaltered antibacterial defense when compared with normal wild-type mice. These data suggest that TLR2 plays a limited role in the innate immune response to pneumococcal pneumonia, and that additional pattern recognition receptors likely are involved in host defense against this common respiratory pathogen.




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