RT Journal Article
SR Electronic
T1 Lipidome profiles of plasma microvesicles differ in experimental cerebral malaria, compared to malaria without neurological complications
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.07.28.224170
DO 10.1101/2020.07.28.224170
A1 Amani M Batarseh
A1 Fatemeh Vafaee
A1 Elham Hosseini-Beheshti
A1 Alex Chen
A1 Amy Cohen
A1 Annette Juillard
A1 Nicholas Henry Hunt
A1 Michael Mariani
A1 Todd Mitchell
A1 Georges Emile Raymond Grau
YR 2020
UL http://biorxiv.org/content/early/2020/07/29/2020.07.28.224170.abstract
AB Cerebral malaria (CM), a fatal complication of Plasmodium infection that affects children in sub-Saharan Africa and adults in South-East Asia, results from incompletely understood pathogenetic mechanisms, which include an excessive release of microvesicles (MV). Plasma MV levels have been found elevated in CM patients and in the experimental mouse model.We compared lipid profiles in circulating MV purified from CBA mice infected with P. berghei ANKA (PbA), which causes CM, to those from P. yoelii (Py), which does not. Here we show that plasma MV produced at the time of CM differed dramatically from those from non-CM mice, in spite of identical levels of parasitaemia. Using high-resolution LCMS, we identified over 300 lipid species within 12 lipid classes. Total lysophosphatidylethanolamine (LPE) levels were significantly lower in PbA infection compared to uninfected mice, while they were unchanged in Py MV, and lysophosphatidylcholine (LPC) was more significantly reduced in PbA mice compared to the other two groups. These results suggest, for the time, that experimental CM is characterised by specific changes in lipid composition of circulating MV, pointing towards triglycerides (TG) especially docosahexaenoic acid (DHA 22:6) containing species, phosphatidylethanolamine (PE), LPC, LPE, and diacylglycerol (DG) as potential important players in CM pathogenesis.Competing Interest StatementThe authors have declared no competing interest.