Gouagna Louis-Clément, Van der Kolk M., Roeffen W., Verhave J. P., Eling W., Sauerwein R., Boudin Christian. (2007). Role of heat-labile serum factor or host complement in the inhibition of Plasmodium falciparum sporogonic stages in Anopheles stephensi by gametocyte carriers' serological factors. Parasitology, 134 (10), p. 1315-1327. ISSN 0031-1820.
Titre du document
Role of heat-labile serum factor or host complement in the inhibition of Plasmodium falciparum sporogonic stages in Anopheles stephensi by gametocyte carriers' serological factors
Gouagna Louis-Clément, Van der Kolk M., Roeffen W., Verhave J. P., Eling W., Sauerwein R., Boudin Christian
Source
Parasitology, 2007,
134 (10), p. 1315-1327 ISSN 0031-1820
This study investigated the significance of serum complement on transmission-reducing activity (TRA) of field sera from 24 infected Plasmodium falciparum gametocyte carriers (from Cameroon) against cultured NF54 P. falciparum. Laboratory-reared Anopheles stephensi were given infectious blood meals prepared either with sera from naive Dutch donor (AB type) or pair-matched field serum samples, both with and without active complement. TRA of serum factors and host complement on mosquito infection rate and oocyst intensity were divided into the various components involved in the early stages of sporogony. The majority (>80%) of sera tested showed positive antibody titres to Pfs230, the relevant complement-dependent target of transmission -reducing mechanisms. Regardless of the presence of active complement, bloodmeals with field sera exhibited significantly lower infection rates and oocyst intensity than the control group. Serological reactivity in Capture-ELISA against Pfs230 was significantly correlated with the reduction of parasite infectivity. Contrary to our expectation, the presence of active complement in the mosquito bloodmeal did not increase parasite losses and therefore the magnitude of transmission reduction by individual immune sera. Our findings on P.falciparum are consistent with previous studies on animal hosts of Plasmodium, indicating that early P.falciparum sporogonic stages may be insensitive to the antibody-dependent pathways of complement in human serum.
