Junaid Quazim Olawale, Khaw Loke Tim, Mahmud Rohela, Ong Kien Chai, Lau Yee Ling, Borade Prajakta Uttam, Liew Jonathan Wee Kent, Sivanandam Sinnadurai, Wong Kum Thong, Vythilingam Indra
Department of Parasitology, Faculty of Medicine, University of Malaya, Lembah Pantai, 50603 Kuala Lumpur, Malaysia - Department of Biological Science, Faculty of Science, Federal University Kashere, Gombe State, Nigeria.
Department of Parasitology, Faculty of Medicine, University of Malaya, Lembah Pantai, 50603 Kuala Lumpur, Malaysia - Department of Pathology, School of Medicine, International Medical University, 57000 Kuala Lumpur, Malaysia.
Parasite. 2017;24:38. doi: 10.1051/parasite/2017040. Epub 2017 Oct 16.
As the quest to eradicate malaria continues, there remains a need to gain further understanding of the disease, particularly with regard to pathogenesis. This is facilitated, apart from in vitro and clinical studies, mainly via in vivo mouse model studies. However, there are few studies that have used gerbils (Meriones unguiculatus) as animal models. Thus, this study is aimed at characterizing the effects of Plasmodium berghei ANKA (PbA) infection in gerbils, as well as the underlying pathogenesis.
Gerbils, 5-7 weeks old were infected by PbA via intraperitoneal injection of 1 × 10 (0.2 mL) infected red blood cells. Parasitemia, weight gain/loss, hemoglobin concentration, red blood cell count and body temperature changes in both control and infected groups were monitored over a duration of 13 days. RNA was extracted from the brain, spleen and whole blood to assess the immune response to PbA infection. Organs including the brain, spleen, heart, liver, kidneys and lungs were removed aseptically for histopathology.
Gerbils were susceptible to PbA infection, showing significant decreases in the hemoglobin concentration, RBC counts, body weights and body temperature, over the course of the infection. There were no neurological signs observed. Both pro-inflammatory (IFNγ and TNF) and anti-inflammatory (IL-10) cytokines were significantly elevated. Splenomegaly and hepatomegaly were also observed. PbA parasitized RBCs were observed in the organs, using routine light microscopy and in situ hybridization.
Gerbils may serve as a good model for severe malaria to further understand its pathogenesis.
随着根除疟疾的探索仍在继续，仍有必要进一步了解该疾病，特别是在发病机制方面。除了体外和临床研究外，这主要通过体内小鼠模型研究来实现。然而，很少有研究使用沙鼠（长爪沙鼠）作为动物模型。因此，本研究旨在描述伯氏疟原虫ANKA株（PbA）感染沙鼠的影响及其潜在的发病机制。
通过腹腔注射1×10（0.2mL）感染的红细胞，对5 - 7周龄的沙鼠进行PbA感染。在13天的时间内，监测对照组和感染组的疟原虫血症、体重增加/减轻、血红蛋白浓度、红细胞计数和体温变化。从脑、脾和全血中提取RNA，以评估对PbA感染的免疫反应。无菌取出包括脑、脾、心、肝、肾和肺在内的器官进行组织病理学检查。
沙鼠对PbA感染敏感，在感染过程中血红蛋白浓度、红细胞计数、体重和体温均显著下降。未观察到神经症状。促炎细胞因子（IFNγ和TNF）和抗炎细胞因子（IL - 10）均显著升高。还观察到脾肿大和肝肿大。使用常规光学显微镜和原位杂交在器官中观察到被PbA寄生的红细胞。
沙鼠可作为重症疟疾的良好模型，以进一步了解其发病机制。
