Analysis of spleen histopathology, splenocyte composition and haematological parameters in four strains of mice infected with Plasmodium berghei K173

Huajing Wang,Guihua Yu,Ji Ma,Tingliang Jiang,Shuo Li,Tingting Qin,Zhao Cui,Hang Shi,Canghai Li,Lanfang Li

doi:10.1186/s12936-021-03786-z

Abstract

BackgroundMalaria is a fatal disease that presents clinically as a continuum of symptoms and severity, which are determined by complex host-parasite interactions. Clearance of infection is believed to be accomplished by the spleen and mononuclear phagocytic system (MPS), independent of artemisinin treatment. The spleen filters infected red blood cells (RBCs) from circulation through immune-mediated recognition of the infected RBCs followed by phagocytosis. This study evaluated the tolerance of four different strains of mice to Plasmodium berghei strain K173 (P. berghei K173), and the differences in the role of the spleen in controlling P. berghei K173 infection.MethodsUsing different strains of mice (C57BL/6, BALB/C, ICR, and KM mice) infected with P. berghei K173, the mechanisms leading to splenomegaly, histopathology, splenocyte activation and proliferation, and their relationship to the control of parasitaemia and host mortality were examined and evaluated.ResultsSurvival time of mice infected with P. berghei K173 varied, although the infection was uniformly lethal. Mice of the C57BL/6 strain were the most resistant, while mice of the strain ICR were the most susceptible. BALB/c and KM mice were intermediate. In the course of P. berghei K173 infection, all infected mice experienced significant splenomegaly. Parasites were observed in the red pulp at 3 days post infection (dpi) in all animals. All spleens retained late trophozoite stages as well as a fraction of earlier ring-stage parasites. The percentages of macrophages in infected C57BL/6 and KM mice were higher than uninfected mice on 8 dpi. Spleens of infected ICR and KM mice exhibited structural disorganization and remodelling. Furthermore, parasitaemia was significantly higher in KM versus C57BL/6 mice at 8 dpi. The percentages of macrophages in ICR infected mice were lower than uninfected mice, and the parasitaemia was higher than other strains.ConclusionsThe results presented here demonstrate the rate of splenic mechanical filtration and that splenic macrophages are the predominant roles in controlling an individual’s total parasite burden. This can influence the pathogenesis of malaria. Finally, different genetic backgrounds of mice have different splenic mechanisms for controlling malaria infection.

Highlights

Malaria is a fatal disease that presents clinically as a continuum of symptoms and severity, which are determined by complex host-parasite interactions
BALB/c, ICR and KM mice developed infection with parasites observed in the blood as early as 1 day post infection, whereas C57BL/6 mice converted at 2 dpi
The percentages of macrophages in ICR infected mice were lower than uninfected mice (Fig. 5D), and the parasitaemia was higher than other strains during the course of P. berghei K173 infection (Fig. 1A)

Summary

Introduction

Malaria is a fatal disease that presents clinically as a continuum of symptoms and severity, which are determined by complex host-parasite interactions. Plasmodium falciparum parasites cause lethal infections worldwide, especially in Africa [1] Reducing this disease burden continues to rely heavily on the availability and proper use of effective anti-malarial drugs. Host immunity and genetic factors are estimated to account for one quarter of the total variability in malaria severity [4, 5]. Host defense mechanisms, such as removal of circulating parasites by the spleen and mononuclear phagocytic system (MPS), are thought to play a major role in rapid control of infection [6], in the presence or absence of artemisinin treatment [7]

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