Elevated IL-17 levels in semi-immune anaemic mice infected with Plasmodium berghei ANKA

Gideon Kofi Helegbe,Mahamoud Sama Cherif,Tetsuo Yanagi,Nguyen Tien Huy,Mohammed Nasir Shuaibu,Mihoko Kikuchi,Kenji Hirayama

doi:10.1186/s12936-018-2257-x

Abstract

BackgroundAlterations in inflammatory cytokines and genetic background of the host contribute to the outcome of malaria infection. Despite the promising protective role of IL-17 in infections, little attention is given to further understand its importance in the pathogenesis of severe malaria anaemia in chronic/endemic situations. The objective of this study, therefore, was to evaluate IL-17 levels in anaemic condition and its association with host genetic factors.MethodsTwo mice strains (Balb/c and CBA) were crossed to get the F1 progeny, and were (F1, Balb/c, CBA) taken through 6 cycles of Plasmodium berghei (ANKA strain) infection and chloroquine/pyrimethamine treatment to generate semi-immune status. Cytokine levels and kinetics of antibody production, CD4+CD25+T regulatory cells were evaluated by bead-based multiplex assay kit, ELISA and FACs, respectively.ResultsHigh survival with high Hb loss at significantly low parasitaemia was observed in Balb/c and F1. Furthermore, IgG levels were two times higher in Balb/c, F1 than CBA. While CD4+CD25+ Treg cells were lower in CBA; IL-4, IFN-γ, IL-12α and IL-17 were significantly higher (p < 0.05) in Balb/c, F1.ConclusionsIn conclusion, elevated IL-17 levels together with high IL-4, IL-12α and IFN-γ levels may be a marker of protection, and the mechanism may be controlled by host factor (s). Further studies of F2 between the F1 and Balb/c will be informative in evaluating if these genes are segregated or further apart.

Highlights

Alterations in inflammatory cytokines and genetic background of the host contribute to the outcome of malaria infection
Though little attention has been given to IL-17 in malaria infection few studies have shown that IL-17 is needed for IL-23 to offer protection against Plasmodium berghei (NK65 strain) infection [13]; significant expansion of IL-17 producing cells correlated to a pro-inflammatory cytokine profile in Plasmodium vivax infection [14]; high IL-17 is associated with high mortality in P. berghei (ANKA strain) infections [15]
Parasitaemia‐time course, profile of haemoglobin loss and erythropoietic response in the semi‐immune ice strains Balb/c, CBA and the cross between them called F1 were taken through five cycles of infection with 104 P. berghei followed by pyrimethamine and chloroquine treatment to generate the semi-immune status

Summary

Introduction

Alterations in inflammatory cytokines and genetic background of the host contribute to the outcome of malaria infection. Several studies have reported on the role played by anti- and pro-inflammatory cytokines in the pathogenesis of malaria [5,6,7,8,9,10,11]. Though little attention has been given to IL-17 in malaria infection few studies have shown that IL-17 is needed for IL-23 to offer protection against Plasmodium berghei (NK65 strain) infection [13]; significant expansion of IL-17 producing cells correlated to a pro-inflammatory cytokine profile in Plasmodium vivax infection [14]; high IL-17 is associated with high mortality in P. berghei (ANKA strain) infections [15]. In addition to its role in host defence against extracellular bacterial infection, IL-17 has been shown to be important in protection against fungal and parasitic infection. The evidence supplied indicates that inhibiting the function of the IL-17 cytokine family could have a beneficial effect on pathogenic conditions in the CNS

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Conclusion