Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

C-reactive protein protects against preerythrocytic stages of malaria.

C-reactive protein protects against preerythrocytic stages of malaria. We previously reported that low doses of interleukin-1 strongly inhibited in vitro development of the hepatic stages of Plasmodium falciparum and P. yoelii. Among several hypotheses, we considered the role of C-reactive protein (CRP), a major acute-phase reactant whose concentration increases markedly in infectious disorders. We demonstrated that human hepatocytes cultured in the presence of interleukin-1 released, as early as 30 min after stimulation, an increased amount of CRP. We then established that CRP bound to the P. falciparum and P. yoelii sporozoite surface membranes, probably via a phosphorylcholine binding site. Experiments in which CRP was added to rat hepatocyte monolayers during or after inoculation confirmed that the target of the CRP-mediated inhibition was at the very early phase of infection. These in vitro functional activities were confirmed in an in vivo model; rats with increased levels of CRP in serum following an injection of turpentine oil were found to be largely protected against an inoculation of P. yoelii sporozoites. The same results were observed in animals inoculated with sporozoites previously incubated in purified CRP or in sera of rats pretreated with turpentine oil. The latter effect was inhibited after incubation of serum from turpentine-injected rats with anti-CRP serum. Infect Immun. 1989 January; 57(1): 278-282 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Infection and Immunity American Society For Microbiology

C-reactive protein protects against preerythrocytic stages of malaria.

C-reactive protein protects against preerythrocytic stages of malaria.

Infection and Immunity , Volume 57 (1): 278 – Jan 1, 1989

Abstract

We previously reported that low doses of interleukin-1 strongly inhibited in vitro development of the hepatic stages of Plasmodium falciparum and P. yoelii. Among several hypotheses, we considered the role of C-reactive protein (CRP), a major acute-phase reactant whose concentration increases markedly in infectious disorders. We demonstrated that human hepatocytes cultured in the presence of interleukin-1 released, as early as 30 min after stimulation, an increased amount of CRP. We then established that CRP bound to the P. falciparum and P. yoelii sporozoite surface membranes, probably via a phosphorylcholine binding site. Experiments in which CRP was added to rat hepatocyte monolayers during or after inoculation confirmed that the target of the CRP-mediated inhibition was at the very early phase of infection. These in vitro functional activities were confirmed in an in vivo model; rats with increased levels of CRP in serum following an injection of turpentine oil were found to be largely protected against an inoculation of P. yoelii sporozoites. The same results were observed in animals inoculated with sporozoites previously incubated in purified CRP or in sera of rats pretreated with turpentine oil. The latter effect was inhibited after incubation of serum from turpentine-injected rats with anti-CRP serum. Infect Immun. 1989 January; 57(1): 278-282

Loading next page...
 
/lp/american-society-for-microbiology/c-reactive-protein-protects-against-preerythrocytic-stages-of-malaria-2nxPhEn5qI

References

References for this paper are not available at this time. We will be adding them shortly, thank you for your patience.

Publisher
American Society For Microbiology
Copyright
Copyright © 1989 by the American Society For Microbiology.
ISSN
0019-9567
eISSN
0019-9567
Publisher site
See Article on Publisher Site

Abstract

We previously reported that low doses of interleukin-1 strongly inhibited in vitro development of the hepatic stages of Plasmodium falciparum and P. yoelii. Among several hypotheses, we considered the role of C-reactive protein (CRP), a major acute-phase reactant whose concentration increases markedly in infectious disorders. We demonstrated that human hepatocytes cultured in the presence of interleukin-1 released, as early as 30 min after stimulation, an increased amount of CRP. We then established that CRP bound to the P. falciparum and P. yoelii sporozoite surface membranes, probably via a phosphorylcholine binding site. Experiments in which CRP was added to rat hepatocyte monolayers during or after inoculation confirmed that the target of the CRP-mediated inhibition was at the very early phase of infection. These in vitro functional activities were confirmed in an in vivo model; rats with increased levels of CRP in serum following an injection of turpentine oil were found to be largely protected against an inoculation of P. yoelii sporozoites. The same results were observed in animals inoculated with sporozoites previously incubated in purified CRP or in sera of rats pretreated with turpentine oil. The latter effect was inhibited after incubation of serum from turpentine-injected rats with anti-CRP serum. Infect Immun. 1989 January; 57(1): 278-282

Journal

Infection and ImmunityAmerican Society For Microbiology

Published: Jan 1, 1989

There are no references for this article.