This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bate, C A Articles by Kwiatkowski, D Search for Related Content PubMed PubMed Citation Articles by Bate, C A Articles by Kwiatkowski, D

research-article

Inhibitory immunoglobulin M antibodies to tumor necrosis factor-inducing toxins in patients with malaria.

Department of Paediatrics, John Radcliffe Hospital, Oxford, United Kingdom.

ABSTRACT

Cytokines such as tumor necrosis factor alpha (TNF) appear to play an important role in the pathogenesis of malaria. We have previously shown that TNF is produced in response to substances released at schizont rupture, which we have called malaria toxins. In mice these toxins stimulate a T cell-independent antibody response, generating short-lived immunoglobulin M (IgM) antibodies that inhibit the TNF-inducing activity of the toxins. We report here that a similar antibody response is seen in humans. Serum from a European adult infected with Plasmodium falciparum inhibited the induction of TNF by malaria toxins derived from P. falciparum-infected erythrocytes. We found that IgM antibodies were responsible for the inhibitory activity. These inhibitory antibodies could not be detected in convalescent-phase serum collected from the same patient 6 weeks later or in sera from healthy European and African controls. The antibodies appeared to be malaria specific in that they inhibited TNF induction by a variety of P. falciparum isolates but failed to inhibit TNF induction by bacterial lipopolysaccharide or lipoteichoic acid. The inhibitory antibodies bound to liposomes containing phosphatidylinositol but not other phospholipids. Serum from a European adult infected with P. vivax also inhibited the activity of toxins derived from P. falciparum-infected erythrocytes, and this too was mediated by IgM antibodies which were malaria specific and bound to phosphatidylinositol liposomes.

This article has been cited by other articles:

• Suguitan, A. L. Jr., Gowda, D. C., Fouda, G., Thuita, L., Zhou, A., Djokam, R., Metenou, S., Leke, R. G. F., Taylor, D. W. (2004). Lack of an Association between Antibodies to Plasmodium falciparum Glycosylphosphatidylinositols and Malaria-Associated Placental Changes in Cameroonian Women with Preterm and Full-Term Deliveries. Infect. Immun. 72: 5267-5273 [Abstract] [Full Text]  
• SEOH, J.-Y., KHAN, M., PARK, S.-H., PARK, H.-K., SHIN, M.-H., HA, E.-H., LEE, B.-E., YOO, K., HAN, H.-S., OH, S., WI, J.-H., HONG, C.-K., OH, C.-H., KIM, Y.-A, PARK, J.-W. (2003). SERUM CYTOKINE PROFILES IN PATIENTS WITH PLASMODIUM VIVAX MALARIA: A COMPARISON BETWEEN THOSE WHO PRESENTED WITH AND WITHOUT HYPERPYREXIA. Am J Trop Med Hyg 68: 102-106 [Abstract] [Full Text]  
• Boutlis, C. S., Gowda, D. C., Naik, R. S., Maguire, G. P., Mgone, C. S., Bockarie, M. J., Lagog, M., Ibam, E., Lorry, K., Anstey, N. M. (2002). Antibodies to Plasmodium falciparum Glycosylphosphatidylinositols: Inverse Association with Tolerance of Parasitemia in Papua New Guinean Children and Adults. Infect. Immun. 70: 5052-5057 [Abstract] [Full Text]  
• Jakobsen, P. H., McKay, V., N'Jie, R., Olaleye, B. O., D'Alessandro, U., Zhang, G.-H., Eggelte, T. A., Koch, C., Greenwood, B. M. (1998). Decreased Antitoxic Activities among Children with Clinical Episodes of Malaria. Infect. Immun. 66: 1654-1659 [Abstract] [Full Text]