| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
*
Division of Clinical Immunology and Rheumatology and
Department of Microbiology, University of Alabama, Birmingham, AL 35294; and
Biomedical Sciences Research Center "A. Fleming," Vari, Greece
The acute-phase response (APR) is regulated by TNF-
, IL-1ß,
and IL-6 acting alone, in combination, or in concert with hormones. The
anaphylotoxin C5a, generated during complement activation, induces in
vitro the synthesis of these cytokines by leukocytes and of acute-phase
proteins by HepG2 cells. However, there is no clear evidence for a role
of C5a or any other complement activation product in regulation of the
APR in vivo. In this study, using human C-reactive protein (CRP)
transgenic mice deficient in C3 or C5, we investigated whether
complement activation contributes to induction of the acute-phase
proteins CRP and serum amyloid P-component (SAP). Absence of C3 or C5
resulted in decreased LPS-induced up-regulation of the
CRP transgene and the mouse SAP gene.
Also, LPS induced both the IL-1ß and
IL-6 genes in normocomplementemic mice, but in
complement-deficient mice it significantly induced only
IL-6. Like LPS injection, activation of complement by
cobra venom factor led to significant elevation of serum CRP and SAP in
normocomplementemic mice but not in complement-deficient mice.
Injection of recombinant human C5a into human CRP transgenic mice
induced the IL-1ß gene and caused significant
elevation of both serum CRP and SAP. However, in human CRP transgenic
IL-6-deficient mice, recombinant human C5a did not induce the
CRP nor the SAP gene. Based on these
data, we conclude that during the APR, C5a generated as a consequence
of complement activation acts in concert with IL-6 and/or IL-1ß to
promote up-regulation of the CRP and SAP
genes.
This article has been cited by other articles:
|
|
 |
|
  E. Paffen and M. P.M. deMaat C-reactive protein in atherosclerosis: A causal factor? Cardiovasc Res, July 1, 2006; 71(1): 30 - 39. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G Zandman-Goddard, M Blank, P Langevitz, L Slutsky, M Pras, Y Levy, O Shovman, T Witte, A Doria, J Rovensky, et al. Anti-serum amyloid component P antibodies in patients with systemic lupus erythematosus correlate with disease activity Ann Rheum Dis, December 1, 2005; 64(12): 1698 - 1702. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Wang, S. Oparil, Y.-F. Chen, M. A. McCrory, G. A. Skibinski, W. Feng, and A. J. Szalai Estrogen Treatment Abrogates Neointima Formation in Human C-Reactive Protein Transgenic Mice Arterioscler Thromb Vasc Biol, October 1, 2005; 25(10): 2094 - 2099. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. E. Lund, K. Schuer, M. Hollifield, T. D. Randall, and B. A. Garvy Clearance of Pneumocystis carinii in Mice Is Dependent on B Cells But Not on P. carinii-Specific Antibody J. Immunol., August 1, 2003; 171(3): 1423 - 1430. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. J. Szalai, S. Nataf, X.-Z. Hu, and S. R. Barnum Experimental Allergic Encephalomyelitis Is Inhibited in Transgenic Mice Expressing Human C-Reactive Protein J. Immunol., June 1, 2002; 168(11): 5792 - 5797. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. H. Eckel, M. Wassef, A. Chait, B. Sobel, E. Barrett, G. King, M. Lopes-Virella, J. Reusch, N. Ruderman, G. Steiner, et al. Prevention Conference VI: Diabetes and Cardiovascular Disease: Writing Group II: Pathogenesis of Atherosclerosis in Diabetes Circulation, May 7, 2002; 105 (18): e138 - e143. [Full Text] [PDF]
|
|
|
|
 |
|
 S. Li, V. M. Holers, S. A. Boackle, and C. M. Blatteis Modulation of Mouse Endotoxic Fever by Complement Infect. Immun., May 1, 2002; 70(5): 2519 - 2525. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
