Purpose

During malarial infection, both parasites and host red blood cells (RBCs) come under severe oxidative stress due to the production of free radicals. The host system responds in protecting the RBCs against the oxidative damage caused by these free radicals by producing antioxidants. In this study, we investigated the antioxidant enzyme; superoxide dismutase (SOD) activity and cytokine interactions with parasitaemia in Ghanaian children with severe and uncomplicated malaria.

Methodology

One hundred and fifty participants aged 0–12 years were administered with structured questionnaires. Active case finding approach was used in participating hospitals to identify and interview cases before treatment was applied. Blood samples were taken from each participant and used to quantify malaria parasitaemia, measure haematological parameters and SOD activity. Cytokine levels were measured by commercial ELISA kits. DNA comet assay was used to evaluate the extent of parasite DNA damage due to oxidative stress.

Results

Seventy – Nine (79) and Twenty- Six (26) participants who were positive with malaria parasites were categorized as severe (56.75 × 10³ ± 57.69 parasites/µl) and uncomplicated malaria (5.87 × 10³ ± 2.87 parasites/µl) respectively, showing significant difference in parasitaemia (p < 0.0001). Significant negative correlation was found between parasitaemia and SOD activity levels among severe malaria study participants (p = 0.0428). Difference in cytokine levels (IL-10) amongst the control, uncomplicated and severe malaria groups was significant (p < 0.0001). The IFN-γ/IL-10 /TNF-α/IL-10 ratio differed significantly between the malaria infected and non- malaria infected study participants. DNA comet assay revealed damage to Plasmodium parasite DNA.

Conclusion

Critical roles played by SOD activity and cytokines as anti-parasitic defense during P. falciparum malaria infection in children were established.

中文翻译：

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加纳儿童严重和无并发症疟疾感染中宿主与寄生虫的相互作用

目的

在疟疾感染期间，寄生虫和宿主红细胞（RBC）都会因自由基的产生而承受严重的氧化应激。宿主系统通过产生抗氧化剂来保护红细胞免受这些自由基引起的氧化损伤。在这项研究中，我们研究了抗氧化酶；超氧化物歧化酶（SOD）活性和细胞因子与患有严重和无并发症的疟疾的加纳儿童寄生虫血症的相互作用。

方法

对 150 名 0-12 岁的参与者进行了结构化问卷调查。参与医院采用主动病例发现方法，在治疗前识别和访谈病例。从每位参与者身上采集血样，用于量化疟原虫血症、测量血液学参数和 SOD 活性。通过商业 ELISA 试剂盒测量细胞因子水平。DNA 彗星测定用于评估氧化应激引起的寄生虫 DNA 损伤的程度。

结果

七十至九 (79) 名和二十六 (26) 名疟疾寄生虫呈阳性的参与者分别被归类为严重疟疾( 56.75 × 10 ³ ± 57.69 寄生虫/μl) 和无并发症疟疾 (5.87 × 10 ³ ± 2.87 寄生虫/μl) ，显示出寄生虫血症的显着差异（p  <0.0001）。在严重疟疾研究参与者中发现寄生虫血症和 SOD 活性水平之间存在显着负相关（p =  0.0428）。对照组、无并发症组和重症疟疾组的细胞因子水平 (IL-10) 差异显着 ( p  < 0.0001)。感染疟疾和未感染疟疾的研究参与者之间的 IFN-γ/IL-10/TNF-α/IL-10 比率存在显着差异。DNA 彗星分析揭示了疟原虫寄生虫 DNA的损伤。

结论

确定了 SOD 活性和细胞因子在儿童恶性疟原虫疟疾感染期间作为抗寄生虫防御所发挥的关键作用。