Papel das citocinas IL-4 e IFN-y na viscosidade do sangue de indivíduos infectados por Plasmodium vivax

Abstract

In Brazil, malaria occurs mostly in the Amazon region and is transmitted in most by Plasmodium vivax. Infections caused by P. vivax has emerged as a potentially lethal condition, and induces greater production of proinflammatory cytokines than P. falciparum. Changes in the morphology of erythrocytes, elevation some biochemical factors and proteins released in the inflammatory process can promote changes in blood viscosity. Being these factors involved in malaria by P. vivax, this study evaluates the viscosity changes in infections by this species and verifies whether increase of Interferon-γ and Interleukin-4, both involved in the pathophysiology of the disease, have a direct relationship in blood viscosity profile. The hypothesis is that the increase in cytokine levels can interfere in the blood viscosity of the host and influence blood flow modification. We used 17 blood samples from symptomatic individuals infected with P. vivax that living in an endemic area (Porto Velho-RO) and 18 samples from individuals of non endemic area who had never been diagnosed with malaria, as a control group. Quantification of cytokines was performed by flow cytometry and measurement of blood viscosity by rheometry. The hematological parameters of individuals infected with P. vivax were within the normal reference values. There was no significant difference in serum levels of Interleukin-4 compared to the control group, already Interferon-γ presented a significant increase in the infected individuals. How much the viscosity, both cytokines promoted an increase, but there was an increase exacerbated in simulations with Interferon-γ, accompanied of the decrease of whole blood fluidity. The fluidity of the whole blood in the simulations performed with Interleukin-4 were similar to the control group. Therefore, it is concluded that the serum elevation of Interleukin-4 does not favor the occurrence of hemodynamic disturbances in P. vivax infections, while Interferon-γ can potentially contribute to the occurrence of these disorders and may be involved in the worsening of the disease.