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*
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.
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