DID YOU KNOW? DTIC has over 3.5 million final reports on DoD funded research, development, test, and evaluation activities available to our registered users. Click
HERE to register or log in.
Accession Number:
ADA280464
Title:
Increased Fibrinogen Synthesis in Mice During the Acute Phase Response: Co-Operative Interaction of Interleukin 1, Interleukin 6, and Interleukin 1 Receptor Antagonist
Descriptive Note:
Corporate Author:
ARMED FORCES RADIOBIOLOGY RESEARCH INST BETHESDA MD
Report Date:
1993-09-01
Pagination or Media Count:
6.0
Abstract:
Interleukin 6 IL-6 stimulates fibrinogen Fg gene expression both in vivo and in vitro while interleukin 1 IL-1 paradoxically stimulates in vivo, yet inhibits in vitro, Fg synthesis. The naturally occurring interleukin 1 receptor antagonist IL-1ra and passive immunization with anti-IL-6 antiserum were used to study the in vivo mechanism of action of IL-1 on Fg gene expression. Changes in plasma FG and hepatic Fg mRNA concentrations were measured following administration of exogenous IL-1ra together with IL-6 or IL-1 to CD2F1 mice. Our results suggest that in vivo, IL-1 per se inhibits Fg production since when IL-14a was co-administered alone. The data suggest that IL-1 stimulates Fg production through intermediate production of IL-6, since stimulation was abrogated when either IL-1ra or anti-IL-6 antiserum was co- administered with IL-1. An in vivo role for IL-1ra in the stimulation of Fg by IL-1 was supported by the observation that within 1 h o IL-1 administration to mice, IL-1ra mRNA was detectable in liver. It appears that IL-1, an early mediator of inflammation, inhibits constitutive expression of Fg genes and stimulates the IL-1ra and IL-6 genes. The inhibitory effect of IL-1 is reversed by endogenous IL-1ra and IL-6 genes. The inhibitory effect of IL-1 is reversed by endogenous IL1ra and by the direct stimulation of Fg gene expression by IL- 6
Distribution Statement:
APPROVED FOR PUBLIC RELEASE
