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The Journal of Immunology, 2002, 168: 372-378.
Copyright © 2002 by The American Association of Immunologists

IL-18 Improves the Early Antimicrobial Host Response to Pneumococcal Pneumonia

Fanny N. Lauw*,{dagger}, Judith Branger*,{dagger}, Sandrine Florquin{ddagger}, Peter Speelman{dagger}, Sander J. H. van Deventer*, Shizuo Akira§ and Tom van der Poll1,*,{dagger}

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

To determine the role of endogenous IL-18 during pneumonia, IL-18 gene-deficient (IL-18-/-) mice and wild-type (WT) mice were intranasally inoculated with Streptococcus pneumoniae, the most common causative agent of community-acquired pneumonia. Infection with S. pneumoniae increased the expression of IL-18 mRNA and was associated with elevated concentrations of both precursor and mature IL-18 protein within the lungs. IL-18-/- mice had significantly more bacteria in their lungs and were more susceptible for progressing to systemic infection at 24 and 48 h postinoculation. Similarly, treatment of WT mice with anti-IL-18 was associated with enhanced outgrowth of pneumococci. In contrast, the clearance of pneumococci from lungs of IL-12-/- mice was unaltered when compared with WT mice. Furthermore, anti-IL-12 did not influence bacterial clearance in either IL-18-/- or WT mice. These data suggest that endogenous IL-18, but not IL-12, plays an important role in the early antibacterial host response during pneumococcal pneumonia.




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