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Infection and Immunity, June 2000, p. 3455-3462, Vol. 68, No. 6
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

A Model for Sequestration of the Transmission Stages of Plasmodium falciparum: Adhesion of Gametocyte-Infected Erythrocytes to Human Bone Marrow Cells

Nicola J. Rogers,dagger Belinda S. Hall,Dagger Jacktone Obiero,§ Geoffrey A. T. Targett, and Colin J. Sutherland*

Immunology Unit, Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London WC1E 7HT, United Kingdom

Received 28 December 1999/Returned for modification 23 February 2000/Accepted 16 March 2000

With the aim of developing an appropriate in vitro model of the sequestration of developing Plasmodium falciparum sexual-stage parasites, we have investigated the cytoadherence of gametocytes to human bone marrow cells of stromal and endothelial origin. Developing stage III and IV gametocytes, but not mature stage V gametocytes, adhere to bone marrow cells in significantly higher densities than do asexual-stage parasites, although these adhesion densities are severalfold lower than those encountered in classical CD36-dependent assays of P. falciparum cytoadherence. This implies that developing gametocytes undergo a transition from high-avidity, CD36-mediated adhesion during stages I and II to a lower-avidity adhesion during stages III and IV. We show that this adhesion is CD36 independent, fixation sensitive, stimulated by tumor necrosis factor alpha, and dependent on divalent cations and serum components. These data suggest that gametocytes and asexual parasites utilize distinct sets of receptors for adhesion during development in their respective sequestered niches. To identify receptors for gametocyte-specific adhesion of infected erythrocytes to bone marrow cells, we tested a large panel of antibodies for the ability to inhibit cytoadherence. Our results implicate ICAM-1, CD49c, CD166, and CD164 as candidate bone marrow cell receptors for gametocyte adhesion.

* Corresponding author. Mailing address: Immunology Unit, Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, Keppel St., London WC1E 7HT, United Kingdom. Phone: 44 (0)171 927 2338. Fax: 44 (0)171 636 8636. E-mail: colin.sutherland{at}lshtm.ac.uk.

dagger Present address: Department of Immunology, Imperial College School of Medicine, Hammersmith Campus, London W12 ONN, United Kingdom.

Dagger Present address: Wellcome Trust Molecular Parasitology Laboratory, Department of Biochemistry, Imperial College, London SW7, United Kingdom.

§ Present address: KEMRI/Wellcome Trust Research Laboratories, Kilifi, Kenya.

Infection and Immunity, June 2000, p. 3455-3462, Vol. 68, No. 6
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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