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.

Allyson Guimarães Da Costa,Maria Izabel Ovellar Hekcmann,Andréa Monteiro Tarragô,Aya Sadahiro,Paulo Afonso Nogueira,Nadja Pinto Garcia,Lis Ribeiro Do Valle Antonelli,Pedro Augusto Carvalho Costa,Maria Do Perpétuo Socorro Lopes Dos Santos,Olindo Assis Martins-Filho,Andréa Teixeira-Carvalho,João Paulo Diniz Pimentel,Adriana Malheiro

doi:10.1155/2014/318250

Abstract

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.

Highlights

Malaria is caused by infection with the protozoan parasite from the gender Plasmodium and affects millions of individuals causing serious morbidity
Malaria is a complex disease that affects approximately 300 million people every year, with the Plasmodium vivax the most geographically widespread species of Plasmodium causing human disease [13, 14]. While they are essential for limiting the parasite load, in almost every infection, proinflammatory biomarkers create a harmful microenvironment in the host, leading to pathology
It has been reported that in severe disease caused by P. vivax, patients produce higher levels of IFN-γ than IL-10, as determined by the ratio between these cytokines [7]

Summary

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. We examined the levels of serum biomarkers and their interaction during acute malaria. Blood samples were collected from P. vivax-infected patients at admission and from healthy donors. 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. 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. 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

Introduction

Results

Discussion