Published ahead of print on December 14, 2006, doi:10.1165/rcmb.2006-0166OC Am. J. Respir. Cell Mol. Biol., Volume 36, Number 5, May 2007, 609-614 A more recent version of this article appeared on May 1, 2007
Submitted on May 9, 2006 Toll-like Receptor2 Does Not Contribute to Host Response During Postinfluenza Pneumococcal PneumoniaMark C Dessing1*,1 Center for Infection and Immunity Amsterdam (CINIMA), University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands; Center for Experimental and Molecular Medicine, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands, 2 Center for Experimental and Molecular Medicine, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands; Laboratory of Experimental Immunology, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands; Department of Pulmonology, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands, 3 Department of Pathology, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands, 4 Exploratory Research for Advanced Technology, Japan Science and Technology Agency, Osaka, Japan * To whom correspondence should be addressed. E-mail: m.c.dessing{at}amc.uva.nl.
Background: Influenza A can be complicated by secondary bacterial pneumonia, which is most frequently caused by Streptococcus (S.) pneumoniae and associated with uncontrolled pulmonary inflammation. Evidence points to Toll-like receptor (TLR) 2 as a possible mediator of this exaggerated lung inflammation: (1) TLR2 is the most important "sensor" for gram-positive stimuli, (2) TLR2 contributes to S. pneumoniae - induced inflammation, and (3) influenza A enhances TLR2 expression in various cell types. Therefore, the objective of this study was to determine the role of TLR2 in the host response to postinfluenza pneumococcal pneumonia. Methods: TLR2 knockout (KO) and wild-type (WT) mice were infected intranasally with influenza A virus. Fourteen days later they were administered with S. pneumoniae intranasally. Results: Influenza was associated with a similar transient weight loss in TLR2 KO and WT mice. Both mouse strains were fully recovered and had completely cleared the virus at day 14. Importantly, no differences between TLR2 KO and WT mice were detected during postinfluenza pneumococcal pneumonia with respect to bacterial growth, lung inflammation and cytokine/chemokine concentrations, with the exception of lower pulmonary levels of cytokine-induced neutrophil chemoattractant in TLR2 KO mice. Conclusion:Toll-like receptor 2 does not contribute to host defense during murine postinfluenza pneumococcal pneumonia.
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