Volume 9 Supplement 2

Parasite to Prevention: Advances in the understanding of malaria

Open Access

Suppression of erythropoiesis by Plasmodium vivax infection

  • Tasanee Panichakul1,
  • Witchuda Payuhakrit2,
  • Chokdee Wongborisuth3,
  • Suradej Hongeng4 and
  • Rachanee Udomsangpetch2
Malaria Journal20109(Suppl 2):P35

https://doi.org/10.1186/1475-2875-9-S2-P35

Published: 20 October 2010

Background

Reports of severe anemia due to P. vivax infection increase [1]. P. vivax is considered to infect reticulocytes and parasitemia is generally low, this suggests that in addition to the simple destruction of infected red cells there is another mechanism to induce anemia in vivax. A report of vivax malaria in bone marrow from severely anemia patients exhibited dyserythropoiesis [2]. Our study demonstrated that P. vivax could infect erythroblasts and erythroblast loss was at least partially attributed to direct killing by parasite invasion [3]. However, the mechanism involving in induction of anemia in vivax malaria is still unclear. Here, hematopoietic stem cells (HSCs)/CD34+ cells from normal human cord blood were subjected to study the suppression of erythropoiesis by P. vivax infection. Erythroid cells derived from HSCs were cultured in serum-free medium supplemented with growth factors and cytokines. Intact or lysed P. vivax-infected erythrocytes (PV-IE) isolated from patient blood were added to erythroid cultures. Results showed both intact and lysed PV-IE could inhibit erythroid expansion by up to 50-55 % compared with controls containing red cells (RBCs) (see Figure 1).
Figure 1

Inhibition of erythroid expansion. HSCs, 5 day-old, 105 cells were cultured with intact or lysed PV-IE and further cultured up to 12 days. Intact and lysed RBCs and TNF-α were as controls.

The reduction of erythroid expansion was not significantly greater by intact PV-IE when compared with lysed PV-IE. The inhibition of cell expressing glyphorin A was up to 66.67 % compared with controls.

Conclusion

P. vivax could inhibit erythroid growth and development and this suppression of erythropoiesis by P. vivax infection is plausible to involve in induction of anemia.

Declarations

Acknowledgements

This was supported by Thailand research fund, Commission on Higher Education, Ministry of Education and Suan Dusit Rajabhat University, Bangkok, Thailand (MRG5380092).

Authors’ Affiliations

(1)
Faculty of Science and Technology, Suan Dusit Rajabhat University
(2)
Department of Pathobiology, Faculty of Science, Mahidol University
(3)
Research Center, Faculty of Medicine, Ramathibodi Hospital, Mahidol University
(4)
Department of Pediatric, Faculty of Medicine, Ramathibodi Hospital, Mahidol University

References

  1. Kochar DK, Das A, Kochar SK, Saxena V, Sirohi P, Garg S, Kochar A, Khatri MP, Gupta V: Severe Plasmodium vivax malaria: a report on serial cases from Bikaner in northwestern India. Am J Trop Med Hyg. 2009, 80: 194-198.PubMedGoogle Scholar
  2. Wickramasinghe SN, Abdalla SH: Blood and bone marrow changes in malaria. Baillieres Best Pract Res Clin Haematol. 2000, 13: 277-299.View ArticlePubMedGoogle Scholar
  3. Panichakul T, Sattabongkot J, Chotivanich K, Sirichaisinthop J, Cui L, Udomsangpetch R: Production of erythropoietic cells in vitro for continuous culture of Plasmodium vivax. Inter J Parasitol. 2007, 37: 1551-1557. 10.1016/j.ijpara.2007.05.009.View ArticleGoogle Scholar

Copyright

© Panichakul et al; licensee BioMed Central Ltd. 2010

This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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