The protective ability of human CRP against
S. pneumoniae type 3 (Pn3) and type 4 (Pn4) infection was studied in an experimental model with the BALB/c mouse.
A single injection of 200μg of CRP 30min prior to intravenous infection protected the mice from Pn3 or Pn4 infection. However, CRP did not protect the mice from lethal infection with
Salmonella typhimurium LT-2, to which CRP did not bind. In dose-response protection experiments using Pn3, injection of 25 to 400μg of CRP per mouse caused a significant decrease in lethality while 12.5μg per mouse was ineffective. In addition, the protection with CRP was also seen in the mice that lacked the antibody to phosphocholine and also in the mice that lacked C3. The clearance studies of CRP showed that more than 95% of CRP injected were cleared from the mouse blood by 24 hours post injection. An injection of CRP 24 hours prior to Pn3 infection failed to protect the mice.
These results suggest that CRP protection not requiring C3, results from an opsonic function specific for
S. pneumoniae.
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