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Infection and Immunity, June 2005, p. 3287-3293, Vol. 73, No. 6
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.6.3287-3293.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Immunohistological Characterization of Macrophage Migration Inhibitory Factor Expression in Plasmodium falciparum-Infected Placentas

Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Public Health Service, U.S. Department of Health and Human Services, Atlanta, Georgia 30333,¹ Center for Tropical and Emerging Global Diseases and Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, Georgia 30602,² Department of Pathology, Egleston Children's Hospital, Emory University School of Medicine, Atlanta, Georgia 30322,³ Vector Biology and Control Research Center, Kenya Medical Research Institute, Kisumu, Kenya,⁴ Atlanta Research and Education Foundation, Atlanta, Georgia 30033,⁵ Department of Microbiology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand,⁶ Roll Back Malaria, World Health Organization, Geneva, Switzerland⁷

Received 18 December 2003/ Returned for modification 16 February 2004/ Accepted 16 January 2005

Previously, we have shown that macrophage migration inhibitory factor (MIF) was highly elevated in the placental intervillous blood (IVB) of Plasmodium falciparum-infected women. Here, we compared the expression of MIF in placental tissues obtained from P. falciparum-infected and -uninfected women. Immunoperoxidase staining showed a consistent pattern of MIF expression in syncytiotrophoblasts, extravillous trophoblasts, IVB mononuclear cells, and amniotic epithelial cells, irrespective of their malaria infection status. Cytotrophoblast, villous stroma, and Hofbauer cells showed focal staining. Only amniotic epithelial and IVB mononuclear cells from P. falciparum-infected placentas exhibited significantly higher level of MIF expression than uninfected placentas. Stimulation of syncytilized human trophoblast BeWo cells with P. falciparum-infected erythrocytes that were selected to bind these cells resulted in significant increases in MIF secretion, whereas control erythrocytes, lipopolysaccharides, and synthetic ß-hematin had minimal effect. These findings suggest that placental malaria modulates MIF expression in different placental compartments.

Editor: W. A. Petri, Jr.

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