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Infection and Immunity, September 2004, p. 5267-5273, Vol. 72, No. 9
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.9.5267-5273.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Lack of an Association between Antibodies to Plasmodium falciparum Glycosylphosphatidylinositols and Malaria-Associated Placental Changes in Cameroonian Women with Preterm and Full-Term Deliveries

Amorsolo L. Suguitan Jr.,1 D. Channe Gowda,2 Genevieve Fouda,1 Lucy Thuita,1 Ainong Zhou,3 Rosine Djokam,4 Simon Metenou,1 Rose G. F. Leke,4 and Diane Wallace Taylor1*

Department of Biology, Georgetown University, Washington, D.C.,1 Department of Biochemistry and Molecular Biology, Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, Hershey, Pennsylvania,2 AZ Data Clinic, Inc., Rockville, Maryland,3 Faculty of Medicine and Biomedical Sciences, Biotechnology Center, University of Yaoundé, Yaoundé, Cameroon4

Received 20 February 2004/ Returned for modification 4 April 2004/ Accepted 4 June 2004

Sequestration of Plasmodium falciparum parasites within the placenta often leads to an accumulation of macrophages within the intervillous space and increased production of tumor necrosis factor alpha (TNF-{alpha}), a cytokine associated with placental pathology and poor pregnancy outcomes. P. falciparum glycosylphosphatidylinositol (GPI) anchors have been shown to be the major parasite component that induces TNF-{alpha} production by monocytes and macrophages. Antibodies against P. falciparum GPI (anti-PfGPI), however, can inhibit the induction of TNF-{alpha} and inflammation. Thus, the study was undertaken to determine whether anti-PfGPI antibodies down-regulate inflammatory-type changes in the placentas of women with malaria. Anti-PfGPI immunoglobulin M (IgM) and IgG levels were measured in 380 pregnant women with or without placental malaria, including those who delivered prematurely and at term. Results showed that anti-PfGPI antibody levels increased with gravidity and age and that malaria infection boosted anti-PfGPI antibodies in pregnant women. However, no association was found between anti-PfGPI antibodies and placental TNF-{alpha} levels or the presence of acute or chronic placental malaria. Furthermore, anti-PfGPI antibody levels were similar in women with preterm and full-term deliveries and were not associated with an increase in infant birth weight. Thus, these results fail to support a strong role for anti-PfGPI antibodies in the prevention of chronic placental malaria infections and malaria-associated poor birth outcomes.

* Corresponding author. Mailing address: Reiss Science Building, Room 406, Department of Biology, Georgetown University, 37th and O Sts., N.W., Washington, D.C. 20057. Phone: (202) 687-5972. Fax: (202) 687-5662. E-mail: taylordw{at}georgetown.edu.

Editor: W. A. Petri, Jr.

Infection and Immunity, September 2004, p. 5267-5273, Vol. 72, No. 9
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.9.5267-5273.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.





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