Adherence to human lung microvascular endothelial cells (HMVEC-L) of Plasmodium vivax isolates from Colombia

Briegel De Las Salas,Fabio Tm Costa,Silvia Blair,Adriana Pabón,Cesar Segura,Stefanie Cp Lopes

doi:10.1186/1475-2875-12-347

Abstract

BackgroundFor years Plasmodium vivax has been considered the cause of benign malaria. Nevertheless, it has been observed that this parasite can produce a severe disease comparable to Plasmodium falciparum. It has been suggested that some physiopathogenic processes might be shared by these two species, such as cytoadherence. Recently, it has been demonstrated that P. vivax-infected erythrocytes (Pv-iEs) have the capacity to adhere to endothelial cells, in which intercellular adhesion molecule-1 (ICAM-1) seems to be involved in this process.MethodsAdherence capacity of 21 Colombian isolates, from patients with P. vivax mono-infection to a microvascular line of human lung endothelium (HMVEC-L) was assessed in static conditions and binding was evaluated at basal levels or in tumor necrosis factor (TNF) stimulated cells. The adherence specificity for the ICAM-1 receptor was determined through inhibition with an anti-CD54 monoclonal antibody.ResultsThe majority of P. vivax isolates, 13 out of 21 (61.9%), adhered to the HMVEC-L cells, but P. vivax adherence was at least seven times lower when compared to the four P. falciparum isolates. Moreover, HMVEC-L stimulation with TNF led to an increase of 1.6-fold in P. vivax cytoadhesion, similar to P. falciparum isolates (1.8-fold) at comparable conditions. Also, blockage of ICAM-1 receptor with specific antibodies showed a significant 50% adherence reduction.ConclusionsPlasmodium vivax isolates found in Colombia are also capable of adhering specifically in vitro to lung endothelial cells, via ICAM-1 cell receptor, both at basal state and after cell stimulation with TNF. Collectively, these findings reinforce the concept of cytoadherence for P. vivax, but here, to a different endothelial cell line and using geographical distinct isolates, thus contributing to understanding P. vivax biology.

Highlights

For years Plasmodium vivax has been considered the cause of benign malaria
Chotivanich et al demonstrated that P. vivax isolates from Thailand have the ability to adhere to chondroitin sulphate A (CSA) and to hyaluronic acid (HA) in placental sections [15,16,17,18]
In 2012, Bernabeu et al reported the participation of vir 14 protein in the adherence to intercellular adhesion molecule-1 (ICAM-1) receptor on the Chinese hamster ovary (CHO) cells transfected with human ICAM-1 (CHO-ICAM-1) cell line [18]

Summary

Introduction

For years Plasmodium vivax has been considered the cause of benign malaria. it has been observed that this parasite can produce a severe disease comparable to Plasmodium falciparum. It has been observed that this species can cause severe disease similar to Plasmodium falciparum and complications caused by P. vivax mono-infection have been described, such as cerebral malaria with et al suggested that pulmonary lesions found in P. vivax malaria could be caused by sequestration of parasitic forms within this organ [14]. In this sense, Carvalho et al reported that P. vivax has the ability to cytoadhere ex vivo to human lung endothelial cells (HLEC) and, to a lesser extent, to placenta cryosections. In 2012, Bernabeu et al reported the participation of vir 14 protein in the adherence to ICAM-1 receptor on the Chinese hamster ovary (CHO) cells transfected with human ICAM-1 (CHO-ICAM-1) cell line [18]

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