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Compensates for the Impaired Host Defense of IL-1 Type I Receptor-Deficient Mice During Pneumococcal Pneumonia1
Departments of
*
Experimental Internal Medicine,
Infectious Diseases, Tropical Medicine, and AIDS, and
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
and IL-1
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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