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Infection and Immunity, December 1999, p. 6596-6602, Vol. 67, No. 12
Unité de Parasitologie
Expérimentale,
Received 17 May 1999/Returned for modification 5 August
1999/Accepted 7 September 1999
We performed ex vivo experiments with Plasmodium
falciparum-infected human placentas from primi- and multigravida
women from Cameroon. All women, independent of their gravida status,
had anti-chondroitin sulfate A (CSA) adhesion antibodies which
cross-reacted with heterologous strains, such as FCR3 and
Palo-Alto(FUP)1, which were selected for CSA binding. These antibodies,
directed against the surface of infected erythrocytes obtained by
flushing with CSA (IRBCCSA), were restricted to the
immunoglobulin G3 isotypes. Massive desequestration of parasites was
achieved with soluble CSA but not with anti-ICAM-1 and anti-CD36
monoclonal antibodies. All of the CSA-flushed parasites were analyzed
immediately by using in vitro assays of binding to Saimiri
brain endothelial cells (SBEC) expressing various adhesion receptors.
Parasites derived from all six placentas displayed the CSA adhesion
phenotype. However, only partial inhibition of adhesion was observed in
the presence of soluble CSA or when Sc1D SBEC were treated with
chondroitinase ABC. These results suggest that an additional adhesive
molecule of IRBCCSA which binds to an unidentified receptor
is present in the placenta. This new phenotype was lost once the
parasites adapted to in vitro culture. We observed additional
differences in the CSA adhesion phenotype between placental parasites
and in vitro-cultured parasites panned on endothelial cells carrying
CSA. The minimum size of fractionated CSA required for a significant
inhibition of placental IRBCCSA adhesion to Sc1D cells was
1 to 2 kDa, which contrasts with the 4-kDa size necessary to reach
equivalent levels of inhibition with panned IRBCCSA of this
phenotype. All placental IRBCCSA cytoadhered to Sc17 SBEC,
which express only the CSA receptor. Panning of IRBCCSA on
these cells resulted in a significant quantitative increase of IRBC
cytoadhering to the CSA of Sc1D cells but did not change their capacity
for adhesion to CSA on normal placenta cryosections. Our results
indicate that the CSA binding phenotype is heterogeneous and that
several distinct genes may encode P. falciparum-CSA ligands with distinct binding properties.
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Ex Vivo Desequestration of Plasmodium
falciparum-Infected Erythrocytes from Human Placenta by
Chondroitin Sulfate A
*
Corresponding author. Mailing address: Unité de
Parasitologie Expérimentale, Faculté de Médecine,
Université de la Méditerranée (Aix-Marseille II),
13385 Marseille Cedex 5, France. Phone: 4-91-32-46-33/35. Fax:
4-91-32-46-34. E-mail: gysin{at}medecine.univ-mrs.fr.
Infection and Immunity, December 1999, p. 6596-6602, Vol. 67, No. 12
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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