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Published on: July 3, 2020
In vitro growth of Plasmodium falciparum in neonatal blood
Ulrich Sauerzopf, Yabo J Honkpehedji, Ayôla A Adgenika
1Department of Medicine I, Division of Infectious Diseases and Tropical Medicine, Medical University of Vienna, Vienna, Austria. michael.ramharter@medizin.uni-tuebingen.de.
Insights
Foetal haemoglobin (HbF) erythrocytes do not inherently inhibit Plasmodium falciparum growth. Maternal and cord plasma, however, significantly reduced parasite growth in vitro, suggesting a role in neonatal malaria protection.
Area of Science:
- Malariology
- Immunology
- Hematology
Background:
- Neonatal malaria protection is often attributed to foetal haemoglobin (HbF) inhibiting Plasmodium falciparum growth.
- Recent findings challenge the notion that HbF intrinsically prevents malaria parasite development.
- This study investigates the role of HbF-containing erythrocytes and maternal plasma in malaria parasite growth.
Purpose of the Study:
- To evaluate the effect of foetal haemoglobin (HbF) erythrocytes on in vitro Plasmodium falciparum growth.
- To assess the impact of maternal plasma on in vitro malaria parasite development.
- To challenge or confirm the protective role of HbF against neonatal malaria.
Main Methods:
- Collected umbilical cord blood and maternal peripheral blood in Gabon.
- Prepared erythrocyte suspensions and plasma from collected samples for in vitro cultures.
- Assessed Plasmodium falciparum growth rates using the HRP2 assay.
Main Results:
- In vitro cultures with foetal erythrocytes showed comparable P. falciparum growth rates to those with maternal erythrocytes.
- Both maternal and foetal plasma significantly reduced in vitro P. falciparum growth compared to a control.
- Foetal erythrocytes were equally permissive to P. falciparum growth as adult erythrocytes in vitro.
Conclusions:
- Foetal haemoglobin (HbF) does not appear to be an intrinsic inhibitor of Plasmodium falciparum growth.
- Maternal and cord plasma may contribute to protection against clinical malaria in neonates.
- Further research is needed to understand the mechanisms of innate and acquired protection against neonatal malaria.
Background:
Children below the age of six months suffer less often from malaria than older children in sub-Saharan Africa. This observation is commonly attributed to the persistence of foetal haemoglobin (HbF), which is considered not to permit growth of Plasmodium falciparum and therefore providing protection against malaria. Since this concept has recently been challenged, this study evaluated the effect of HbF erythrocytes and maternal plasma on in vitro parasite growth of P. falciparum in Central African Gabon.
Methods:
Umbilical cord blood and peripheral maternal blood were collected at delivery at the Albert Schweitzer Hospital in Gabon. Respective erythrocyte suspension and plasma were used in parallel for in vitro culture. In vitro growth rates were compared between cultures supplemented with either maternal or cord erythrocytes. Plasma of maternal blood and cord blood was evaluated. Parasite growth rates were assessed by the standard HRP2-assay evaluating the increase of HRP2 concentration in Plasmodium culture.
Results:
Culture of P. falciparum using foetal erythrocytes led to comparable growth rates (mean growth rate = 4.2, 95% CI: 3.5 - 5.0) as cultures with maternal red blood cells (mean growth rate =4.2, 95% CI: 3.4 - 5.0) and those from non-malaria exposed individuals (mean growth rate = 4.6, 95% CI: 3.8 - 5.5). Standard in vitro culture of P. falciparum supplemented with either maternal or foetal plasma showed both significantly lower growth rates than a positive control using non-malaria exposed donor plasma.
Conclusions:
These data challenge the concept of HbF serving as intrinsic inhibitor of P. falciparum growth in the first months of life. Erythrocytes containing HbF are equally permissive to P. falciparum growth in vitro. However, addition of maternal and cord plasma led to reduced in vitro growth which may translate to protection against clinical disease or show synergistic effects with HbF in vivo. Further studies are needed to elucidate the pathophysiology of innate and acquired protection against neonatal malaria.
