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Toll-Like Receptor 2 Does Not Contribute to Host Response during Postinfluenza Pneumococcal Pneumonia

Center for Infection and Immunity Amsterdam (CINIMA); Center for Experimental and Molecular Medicine; Laboratory of Experimental Immunology; Department of Pulmonology; and Department of Pathology, Academic Medical Center, University of Amsterdam, The Netherlands; and Exploratory Research for Advanced Technology, Japan Science and Technology Agency, Osaka, Japan

Correspondence and requests for reprints should be addressed to Mark C. Dessing, Academic Medical Center, Laboratory of Experimental Internal Medicine, Room F0-117, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. E-mail: m.c.dessing{at}amc.uva.nl

Influenza A can be complicated by secondary bacterial pneumonia, which is most frequently caused by Streptococcus 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. 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. 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, or cytokine/chemokine concentrations, with the exception of lower pulmonary levels of cytokine-induced neutrophil chemoattractant in TLR2 KO mice. Toll-like receptor 2 does not contribute to host defense during murine postinfluenza pneumococcal pneumonia.

Key Words: influenza A • Streptococcus pneumoniae • pneumonia • Toll-like receptor • mice

CLINICAL RELEVANCE Postinfluenza pneumococcal pneumonia is associated with stronger inflammatory response than primary pneumonia. We show that TLR2 does not contribute to pulmonary inflammation during postinfluenza pneumococcal pneumonia.

 

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