Background. Recent studies have shown that the inflammatory process, including the biomarker production, and the intense activation of innate immune responses are greater in the malaria caused by Plasmodium vivax than other species. Here, we examined the levels of serum biomarkers and their interaction during acute malaria. Material and Methods. Blood samples were collected from P. vivax-infected patients at admission and from healthy donors. Levels of serum biomarkers were measured by Cytometric Bead Assay or ELISA. Results. P. vivax infection triggered the production of both inflammatory and regulatory biomarkers. Levels of IL-6, CXCL-8, IFN-γ, IL-5, and IL-10 were higher in P. vivax-infected patients than in healthy donors. On the other hand, malaria patients produced lower levels of TNF-α, IL-12p70, and IL-2 than healthy individuals. While the levels of IL-10 and IL-6 were found independent on the number of malaria episodes, higher levels of these cytokines were seen in patients with higher parasite load. Conclusion. A mixed pattern of proinflammatory and regulatory biomarkers is produced in P. vivax malaria. Analysis of biomarker network suggests that IL-10 and IL-6 are a robust axis in malaria patients and that this interaction seems to be associated with the parasite load.
The Robust and Modulated Biomarker Network Elicited by the Plasmodium vivax Infection Is Mainly Mediated by the IL-6/IL-10 Axis and Is Associated with the Parasite Load
A. Guimarães da Costa,Lis Ribeiro do Valle Antonelli,Pedro Augusto Carvalho Costa,João Paulo Diniz Pimentel,N. Garcia,Andréa Monteiro Tarragô,Maria do Perpétuo Socorro Lopes dos Santos,P. Nogueira,Maria Izabel Ovellar Hekcmann,A. Sadahiro,A. Teixeira-Carvalho,O. Martins-Filho,Adriana Malheiro
Published 2014 in Journal of Immunological Research
ABSTRACT
PUBLICATION RECORD
- Publication year
2014
- Venue
Journal of Immunological Research
- Publication date
2014-03-18
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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