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Plasmodium falciparum malaria infection induces elevated blood levels of both total immunoglobulin and anti-plasmodial antibodies belonging to different isotypes. We have previously shown that donors living in areas of malaria transmission develop malaria-specific IgE antibodies that are present at highest concentrations in patients with severe disease, suggesting a role for this isotype in malaria pathogenesis. To establish the possible importance of IgE in the course and severity of this disease, we have analyzed a large and homogenous group of African children (age range = 6 months to 15 years) belonging to one ethnic group (Mossi) living in identical epidemiologic conditions in the same urban area (Ougadougo) of Burkina Faso. While IgG antibodies to P. falciparum increased to high concentrations in very young children and then remained at these levels in older patients, IgE antibodies increased with age, becoming most significantly elevated in children more than four years of age. In older children, those with severe malaria had significantly higher IgE antibody levels than those with non-severe disease. No significant differences between the patient groups were seen for IgG antibodies to P. falciparum. However, when the patients with severe malaria were divided into two groups distinguished by the presence of absence of coma, both IgG and IgE antibodies against malaria were lower in the comatous patients than in the non-comatous patients The results support the conclusion that IgE antibodies against malaria, regardless of their possible protectivity, also contribute to disease severity in this large and homogenous group of African children.
Received June 5, 2002. Accepted for publication April 12, 2003.
Acknowledgements: We thank all the children and parents who participated in this study for their understanding and assistance. We are indebted to the pediatric and laboratory staff of the Centre Hospitalier National Yalgado Ouédraogo in Ouagadougou, Burkina Faso, for continuous and skilful technical assistance. This study was conducted at the Centre National de Recherche et Formation sur le Paludisme of the Ministry of Health of Burkina Faso. The excellent technical assistance of M. Hagstedt is gratefully acknowledged.
Financial support: This study was supported by the Programma di Assistenza Tecnica della Direzione General e per la Cooperazione allo Sviluppo of the Italian Ministry of Foreign Affairs, the Swedish Development Agency (Sida/SAREC), the Swedish Medical Research Council (MFR), the UNDP/World Bank/WHO Special Program for Research and Training in Tropical Diseases (TDR), the Bergvalls Foundation, and the International Collaboration with Developing Countries ( INCO-DC) European Union contract no. IC 18-CT 980361.
Authors’ addresses: Carlo Calissano and David Modiano, Institute of Parasitology, University La Sapienza, Piazzale Aldo Moro 5, 00185 Rome, Italy. Bienveno Sodiomon Sirima and Amadou Konate, Centre National de Recherche et de Formation sur le Paludisme, Ministère de la Santé, 01 BP 2208, Ouagadougo 01, Burkina Faso. Issa Sanou and Alphonse Sawadogo, Centre Hospitalier National Ouedraogo, 03 BP 7022, Ouagadougo 03, Burkina Faso. Hedvig Perlmann, Marita Troye-Blomberg, and Peter Perlmann The Wenner-Gren Institute, Department of Immunology, Stockholm University, SE-10691 Stockholm, Sweden.
Reprint requests: Marita Troye-Blomberg, The Wenner-Gren Institute, Department of Immunology, Stockholm University, SE-10691 Stockholm, Sweden, Telephone: 46-8-164-164, Fax: 46-8-157-356, E-mail: marita{at}imun.su.se.
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