The influence of ABO blood groups system on erythrophagocytosis mediated by IgGs and IgMs from anemic malaria vivax patients
Background: During Plasmodium vivax infections the most common clinical condition is anemia. Despite this huge importance there are few studies in this field and hence, the etiology of anemia is still unknow. Unlike Plasmodium falciparum infections, where this condition is caused mostly by the destruction of infected Red Blood Cells (iRBCs) during the life cycle of the parasite, P. vivax colonizes reticulocytes whose destruction is not sufficient to cause anemia. Therefore the levels of patients haemoglobin drop because there are a massive destruction of non-infected RBCs (nRBCs). Previous studies of our group have shown that erythrophagocytosis of nRBCs is enhanced when these cells are coated with IgGs from anemic patients. These IgGs are autoantibodies directed against RBCs membrane surface proteins and we have also shown that this antibodies are raised during P. vivax infections in anemic patients. Thus, we suggested that erythrophagocytosis of these nRBCs coated with self-antibodies IgGs is a mechanism that may lead to anemia. According to these previous results, the aim of this study is to observe whether the ABO blood system can influence this mechanism, since many of the P. falciparum data revealed the blood group O as protector agaisnt severe malaria and A like gravity intensifier of the disease. In addition the role of IgM was evaluated. Materials and Methods: The nRBCs were collected by venous puncture on the day of the erythrophagocytosis assay from 30 non-infected individuals resident in non-endemic areas. For erythrophagocytosis assay, human monocytic THP-1 cells were grewn on RPMI-1640 medium and 72 hours before the assay they were activated to differentiation to macrophage. The nRBCs were washed, opsonized with IgGs or IgMs purified from sera of anemic and non-anemic malaria vivax patients and healthy individuals and then incubated with activated THP-1. After 2 hours the slides were washed, fixed with methanol, stained with Giemsa and visualized under the optical microscope. Results and conclusions: Our results demonstratet that nRBCs coated with purified IgGs from anemic malaria vivax patients exhibit different erythrophagocytosis rates according with blood types. The most expressive erythrophagocytosis rate was observed for nRBCs belonging to blood group O, followed by B nRBCs and A nRBCs. It was not observed differences on erythrophagocytosis rates from nRBCs coated with IgMs from anemic malaria vivax patients. In this way it is concluded that O nRBCs are more susceptible to erythrofagocytosis in vitro when coated with IgGs from anemic malaria vivax patients than B nRBCs or A nRBCs. IgM appears to be not involved on this mechanism. As erythrophagocytosis seems to be an expressive mechanism that leads to anemia, we supposed that ABO blood group system can influence anemia vivax.