Toll-Like Receptor 2 Plays a Role in the Early Inflammatory Response to Murine Pneumococcal Pneumonia but Does Not Contribute to Antibacterial Defense
Sylvia Knapp,Catharina W. Wieland,Cornelis van 't Veer,Osamu Takeuchi,Shizuo Akira,Sandrine Florquin,Tom van der Poll +6 more
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TLDR
The 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.Abstract:
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.read more
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Journal ArticleDOI
Pathogenesis, treatment, and prevention of pneumococcal pneumonia.
Tom van der Poll,Steven M. Opal +1 more
TL;DR: Versatility of the genome of pneumococci and the bacteria's polygenic virulence capabilities show that a multifaceted approach with many vaccine antigens, antibiotic combinations, and immunoadjuvant therapies will be needed to control this microbe.
Journal ArticleDOI
The gut microbiota plays a protective role in the host defence against pneumococcal pneumonia
Tim J. Schuijt,Jacqueline M. Lankelma,Brendon P. Scicluna,Felipe De Sousa E Melo,Joris J. T. H. Roelofs,J. Daan de Boer,AJ Hoogendijk,Regina de Beer,Alex F. de Vos,Clara Belzer,Willem M. de Vos,Tom van der Poll,W. Joost Wiersinga +12 more
TL;DR: It is found that the gut microbiota protects the host during pneumococcal pneumonia, as reflected by increased bacterial dissemination, inflammation, organ damage and mortality in microbiota-depleted mice compared with controls.
Journal ArticleDOI
Acute Lower Respiratory Tract Infection
TL;DR: This review emphasizes the roles of inflammation and the response of the innate immune system and explains how these two processes interact to rid the lung of microbes but also how they can bring the elimination of infection in the lung to a perilous climax.
Journal ArticleDOI
Selective predisposition to bacterial infections in IRAK-4–deficient children: IRAK-4–dependent TLRs are otherwise redundant in protective immunity
Cheng-Lung Ku,Horst von Bernuth,Horst von Bernuth,Capucine Picard,Shen-Ying Zhang,Huey Hsuan Chang,Kun Yang,Maya Chrabieh,Andrew C. Issekutz,Coleen K. Cunningham,John I. Gallin,Steven M. Holland,Chaim M. Roifman,Stephan Ehl,Joanne Smart,Mimi L.K. Tang,Franck J. Barrat,Ofer Levy,Douglas R. McDonald,Noorbibi K. Day-Good,Richard L. Miller,Hidetoshi Takada,Toshiro Hara,Sami Al-Hajjar,Abdulaziz Al-Ghonaium,David P. Speert,Damien Sanlaville,Xiaoxia Li,Frederic Geissmann,Eric Vivier,László Maródi,Ben Zion Garty,Helen Chapel,Carlos Rodríguez-Gallego,Xavier Bossuyt,Laurent Abel,Anne Puel,Jean-Laurent Casanova +37 more
TL;DR: The IRAK-4–dependent TLRs and IL-1Rs are therefore vital for childhood immunity to pyogenic bacteria, particularly Streptococcus pneumoniae, and appear to play a redundant role in protective immunity to most infections.
Journal ArticleDOI
Toll-like receptors in central nervous system glial inflammation and homeostasis.
TL;DR: This review summarizes the experimental evidence demonstrating a role for TLRs in the context of CNS inflammation in both infectious and noninfectious conditions.
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