Inflammatory immune mediators and Plasmodium falciparum infection: a cross-sectional study among Sudanese patients with severe and uncomplicated malaria

Dia Aldeen Alfaki, M. Hussein, Mustafa Hassan, Amanda G. Eloraish, M. M. Elbasheir
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Abstract

Aim: A number of questions remain unanswered concerning how infected individuals regulate their immune response to Plasmodium falciparum (P. falciparum) parasites at varying levels of exposure. Due to the interactions of inflammatory mediators and cytokines with the P. falciparum parasite complex density, several mediators influence parasitaemia and may give some indications of disease severity and represent effective signs in clinical manifestations of malaria disease. Methods: In this study, various levels of immune response mediators of interleukin 8 (IL-8), tumor necrosis factor-beta (TNF-β, also known as lymphotoxin-α), interferon-gamma (IFN-γ), IL-6, and IL-10 were investigated to the different phases of infection with P. falciparum in hyperendemic states in Sudan (White Nile, Blue Nile). This study vetted the association between certain inflammatory mediators during malaria infection and parasite density. This study was based on a total of 108 cases, in which 86 patients (62.0%) were uncomplicated and (17.6%) were severe, all met the diagnostic criteria and were clinically admitted for malaria infections. Commercial enzyme-linked immunosorbent assay (ELISA) kits were employed to determine the inflammatory mediator’s serum concentration. Results: The analysis of data indicated that older infected children had substantially raised levels of IFN-γ (P < 0.05), among study groups, levels of IFN-γ, TNF-β, and IL-8 were strongly linked with the severity of malaria, in severe and uncomplicated cases (P < 0.001), IL-6 and IL-10 were significantly associated with severe malaria cases uniquely (P < 0.001). Furthermore, we reported a positive correlation between IL-8 and TNF-β during all infection cases (r = 0.760, P < 0.001), Additionally, in severe malaria cases IL-6 was positively correlated with IL-10 (r = 0.575, P = 0.010). Conclusions: Eliminating P. falciparum blood-stage infection needs effective, specific, and tuned immune response strategies. which may present in the mediator’s correlations and depend on the density of the infection. Besides the effective levels contribution of certain cytokines that play protective roles during different stages of an infection.
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炎症免疫介质和恶性疟原虫感染:苏丹严重和无并发症疟疾患者的横断面研究
目的:关于感染个体如何在不同暴露水平下调节其对恶性疟原虫(恶性疟原虫)寄生虫的免疫反应,许多问题仍未得到解答。由于炎症介质和细胞因子与恶性疟原虫寄生虫复合体密度的相互作用,几种介质影响寄生虫血症,可能给出疾病严重程度的一些指示,并代表疟疾疾病临床表现的有效迹象。方法:在本研究中,研究了不同水平的免疫反应介质白细胞介素8 (IL-8)、肿瘤坏死因子-β (TNF-β,也称为淋巴素-α)、干扰素-γ (IFN-γ)、IL-6和IL-10在苏丹(白尼罗河、青尼罗河)高流行州恶性疟原虫感染不同阶段的免疫反应。本研究审查了疟疾感染过程中某些炎症介质与寄生虫密度之间的关系。本研究共纳入108例病例,其中86例(62.0%)无并发症,重症(17.6%)符合诊断标准,均因疟疾感染住院。采用商用酶联免疫吸附试验(ELISA)试剂盒测定炎症介质的血清浓度。结果:数据分析表明,年龄较大的感染儿童的IFN-γ水平显著升高(P < 0.05),在研究组中,IFN-γ、TNF-β和IL-8水平与疟疾的严重程度密切相关(P < 0.001),在严重和无并发症的病例中,IL-6和IL-10仅与严重疟疾病例显著相关(P < 0.001)。此外,在所有感染病例中,IL-8与TNF-β呈正相关(r = 0.760, P < 0.001),在重症疟疾病例中,IL-6与IL-10呈正相关(r = 0.575, P = 0.010)。结论:消除恶性疟原虫血期感染需要有效、特异性和调整的免疫反应策略。这可能存在于介质的相关性中,并取决于感染的密度。除了在感染的不同阶段发挥保护作用的某些细胞因子的有效水平贡献外。
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