Journal article
Loss of complement regulatory proteins on uninfected erythrocytes in vivax and falciparum malaria anemia
DA Oyong, E Kenangalem, JR Poespoprodjo, JG Beeson, NM Anstey, RN Price, MJ Boyle
Jci Insight | AMER SOC CLINICAL INVESTIGATION INC | Published : 2018
Open access
Abstract
Anemia is a major complication of malaria, driven largely by loss of uninfected RBCs during infection. RBC clearance through loss of complement regulatory proteins (CRPs) is a significant contributor to anemia in Plasmodium falciparum infection, but its role in Plasmodium vivax infection is unknown. CRP loss increases RBC susceptibility to macrophage clearance, a process that is also regulated by CD47. We compared CRPs and CD47 expression on infected and uninfected RBCs in adult patients with vivax and falciparum malaria and different anemia severities from Papua, Indonesia. Complement activation and parasite-specific complement-fixing antibodies were measured by ELISA. Levels of CR1 and CD5..
View full abstractGrants
Awarded by National Health and Medical Research Council
Funding Acknowledgements
We thank the Australian Red Cross Bank (Darwin) for providing RBCs for parasite culture and Mary Galinski (Emory University) for providing the recombinant PvMSP3 alpha protein. We thank the staff of the Papuan Health and Community Development Foundation and all staff and teams from previous NO, in vitro, and ACT efficacy studies. We thank Yati Soenarto and Yodi Mahendradhata from the Faculty of Medicine, University of Gadjah Mada, Yogyakarta, for their excellent support to the study. This work was supported by the National Health and Medical Research Council of Australia (International Collaborative Research Grant 283321 to RNP; Early Career Fellowship 1071736, Career Development Award 1141278, and Project Grant 1125656 to MJB; Senior Principal Research Fellowship 1042072 and 1135820 to NMA; Program Grant 290208; and Senior Research Fellowship 1077636 to JGB); Wellcome Trust (International Collaborative Research Grant ME928457MES; Senior Fellowship 200909 to RNP); Charles Darwin University (PhD scholarship to DAO), Menzies School of Health Research (PhD top-up award to DAO), and NIH grant 5RO1 A1041764-08. The Burnet Institute is supported by the National Health and Medical Research Council for Independent Research Institutes Infrastructure Support Scheme and the Victorian State Government Operational Infrastructure Support.