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Department of Rheumatology, Göteborg University, Göteborg, Sweden
IL-1R-deficient mice (IL-1R-/-) and their wild-type
controls (IL-1R+/+) were i.v. inoculated with 1 x
107 or 106 Staphylococcus aureus
per mouse to mimic bacterial sepsis and septic arthritis. The disease
outcome was severely worsened in the IL-1R-/- mice as
compared with IL-1R+/+ mice. Indeed, 3 days after
inoculation of 107 S. aureus per mouse 84%
of IL-1R-/- mice displayed clinical signs of septicemia
as compared with none of the IL-1R+/+ mice. On day 9 after
inoculation with 106 S. aureus per mouse
75% of the IL-1R-/- mice were dead as compared with none
of the IL-1R+/+ mice. Also, the number of staphylococci in
circulation was 25- to 30-fold increased in IL-1R-/- mice
as compared with IL-1R+/+ mice, the most probable reason
for the outcome. The frequency and severity of septic arthritis were
significantly increased in IL-1R-/- mice, as compared
with IL-1R+/+ mice, following i.v. inoculation of
staphylococci. This was probably due to an increased accumulation of
bacteria in the joints of IL-1R-/- mice as compared with
their wild-type controls. Interestingly, while serum levels of IL-18 in
IL-1R-/- mice were significantly lower than in
IL-1R+/+ mice 24 h after inoculation of S.
aureus, both IL-18 and IL-1
were significantly increased in
IL-1R-/- vs IL-1R+/+ mice 4 days after the
bacterial inoculation. In conclusion, IL-1R signaling plays a crucial
role in host protection during systemic S. aureus
infection as seen by the fatal outcome of S. aureus
sepsis and arthritis in IL-1R-deficient mice.
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