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The Journal of Immunology, 2001, 167: 5240-5246.
Copyright © 2001 by The American Association of Immunologists

TNF-{alpha} Compensates for the Impaired Host Defense of IL-1 Type I Receptor-Deficient Mice During Pneumococcal Pneumonia1

Anita W. Rijneveld2,*,{dagger}, Sandrine Florquin{ddagger}, Judith Branger*,{dagger}, Peter Speelman{dagger}, Sander J. H. Van Deventer* and Tom van der Poll*,{dagger}

Departments of * Experimental Internal Medicine, {dagger} Infectious Diseases, Tropical Medicine, and AIDS, and {ddagger} Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

To determine the role of IL-1 in the host defense against pneumonia, IL-1R type I-deficient (IL-1R-/-) and wild-type (Wt) mice were intranasally inoculated with Streptococcus pneumoniae. Pneumonia resulted in elevated IL-1{alpha} and IL-1{beta} mRNA and protein levels in the lungs. Survival rates did not differ between IL-1R-/- and Wt mice after inoculation with 5 x 104 or 2 x 105 CFU. At early time points (24 and 48 h) IL-1R-/- mice had 2-log more S. pneumoniae CFU in lungs than Wt mice; at 72 h bacterial outgrowth in lungs was similar in both groups. Upon histopathologic examination IL-1R-/- mice displayed a reduced capacity to form inflammatory infiltrates at 24 h after the induction of pneumonia. IL-1R-/- mice also had significantly less granulocyte influx in bronchoalveolar lavage fluid at 24 h after inoculation. Since TNF is known to enhance host defense during pneumonia, we determined the role of endogenous TNF in the early impairment and subsequent recovery of defense mechanisms in IL-1R-/- mice. All IL-1R-/- mice treated with anti-TNF rapidly died (no survivors (of 14 mice) after 4 days), while 10-day survival in IL-1R-/- mice (control Ab), Wt mice (anti-TNF), and Wt mice (control Ab) was 7 of 13, 3 of 14, and 12 of 13, respectively. These data suggest that TNF is more important for host defense against pneumococcal pneumonia than IL-1, and that the impaired early host defense in IL-1R-/- mice is compensated for by TNF at a later phase.




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