Coenzyme Q10 Protect Mice Against Inflammatory Responses During Experimental Cerebral Malaria

James Nyabuga Nyariki ,Daniel Mokaya ,Nemwel O Nyamweya ,A Hoerauf ,Ngalla E Jillani ,Alfred Isaac

doi:10.7176/jnsr/9-2-05

Abstract

Malaria is a life threatening infectious diseases transmitted by the bite of infected female Anopheles mosquito and responsible for high morbidity and mortality rates. Cerebral malaria is a complex neurological syndrome, whose pathology is mediated by inflammatory processes triggered by the immune system of the host following infection with Plasmodium falciparum. Coenzyme Q10 is an obligatory cofactor in the electron transport chain. The reduced form of Coenzyme Q10 serves as a potent antioxidant additionally; Coenzyme Q10 has been identified as a modulator of gene expression, inflammation and apoptosis. However, the modulatory effects of Coenzyme Q10 Plasmodium berghei ANKA infection process and risk occurrence of experimental cerebral malaria (ECM) have not been determined. The aim of this study was to elucidate the putative impact of oral administration of Coenzyme-Q10 on the initiation or regulation of inflammatory immune response in ECM of C57BL/6 mice during Plasmodium berghei ANKA (PbA) infection. We observed that oral administration of Coenzyme-Q10 both before and after PbA infection significantly hampered infiltration of inflammatory monocytes into the brain. Furthermore, pro-inflammatory cytokine TNF-α, which is associated with inflammation during ECM, was down-regulated in Coenzyme-Q10 administered mice. Remarkably, Coenzyme-Q10 was very effective in inhibiting dendritic cell differentiation. These data collectively demonstrated the immuno-modulatory function of Coenzyme-Q10 on host inflammatory responses during ECM. Keywords: Plasmodium berghei ANKA, Coenzyme Q10, experimental cerebral malaria DOI : 10.7176/JNSR/9-2-05

Highlights

Malaria is considered a major health burden which continues to claim many lives globally; in 2017 alone there were estimated 219 million cases and 435,000 related deaths, majority of these cases occurred in subSaharan Africa (WHO, 2018)
It was observed that blood parasitemia levels were not significantly changed in mice supplemented with Coenzyme-Q10 compared with wild type (WT) Plasmodium berghei ANKA (PbA)-infected mice (Fig. 1A)
This is consistent with other studies that demonstrated no correlation between blood parasitemia levels and survival from experimental cerebral malaria (ECM) (Dende et al, 2015; Gordon et al, 2015)

Summary

Introduction

Malaria is considered a major health burden which continues to claim many lives globally; in 2017 alone there were estimated 219 million cases and 435,000 related deaths, majority of these cases occurred in subSaharan Africa (WHO, 2018). Malaria is transmitted by the bites of female anopheles mosquitoes; the major pathogens that are known to cause human disease include P. vivax, P. malariae, P. ovale, P. knowlesi and P. falciparum. The chief malaria complication is cerebral malaria which is caused by P. falciparum; and is a severe clinical neurological syndrome that affects pregnant women and children under the age of 5 years (WHO, 2016). Despite treatment with current adjunct antimalarial drugs being in place, it is estimated that 15-25% children die of the disease (WHO, 2014). It has been shown that children who survive from CM develop neurological sequelae, blindness and cognitive impairment (Mishra and Newton, 2009). This presents a big challenge to the management of CM. There is paucity of data on molecular events that contribute to the pathophysiology of the disease

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