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Infection and Immunity, October 2000, p. 5652-5656, Vol. 68, No. 10
Division of Clinical Immunology and
Rheumatology, Department of Medicine,1 and
Department of Microbiology,2 The
University of Alabama at Birmingham, Birmingham, Alabama 35294, and
Biomedical Sciences Research Center "A. Fleming," 16672 Vari, Greece3
Received 8 March 2000/Returned for modification 30 May
2000/Accepted 18 July 2000
C-reactive protein (CRP) is an acute-phase protein with a
well-known association with infection and other inflammatory
conditions. We have shown that expression of human CRP by CRP
transgenic (CRPtg) mice is protective against lethal infection by
Streptococcus pneumoniae, an effect likely mediated by
CRP's ability to bind to this gram-positive pathogen. In the present
study we tested whether CRPtg mice are resistant to infection with
Salmonella enterica serovar Typhimurium, a gram-negative
pathogen that causes the murine equivalent of typhoid fever. CRPtg mice
experimentally infected with a virulent Typhimurium strain lived longer
and had significantly lower mortality than their non-tg littermates.
The greater resistance of CRPtg mice could be attributed to
significantly increased early (0 to 4 h) blood clearance of
salmonellae and significantly decreased numbers of bacteria in the
liver and spleen on day 7 postinfection. In addition, 14 days after
infection with an avirulent Salmonella strain, the serum
titer of anti-Salmonella immunoglobulin G antibodies was
higher in CRPtg than non-tg mice. This study provides unequivocal evidence that CRP plays an important role in vivo in host defense against salmonellae during the early stages of infection. In addition, as the beneficial effect of CRP includes enhancement of the host's humoral immune response, CRP may also contribute indirectly to host
defense during later stages of infection.
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Human C-Reactive Protein Is Protective against
Fatal Salmonella enterica Serovar Typhimurium Infection in
Transgenic Mice
and
*
Corresponding author. Mailing address: Division of
Clinical Immunology & Rheumatology, University of Alabama at
Birmingham, Birmingham, AL 35294. Phone: (205) 975-6241. Fax: (205)
934-1564. E-mail: Alex.Szalai{at}ccc.uab.edu.
Present address: Biomedical Sciences Research Center "A.
Fleming," 16672 Vari, Greece.
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