Barasa M, Ng'ang'a Z W, Sowayi G A, Okoth J M, Barasa M B O, Namulanda F B M, Kagasi E A, Gicheru M M, Ozwara S H
Department of Medical Laboratory Sciences, School of Health Sciences, Masinde Muliro University of Science and Technology (MMUST), P. O. Box 190-50100, Kakamega, Kenya ; Department of Tropical and Infectious Diseases (TID), Institute of Primate Research (IPR) P. O. Box 24481-00502 Karen, Nairobi, Kenya.
Department of Medical Laboratory Sciences, Jomo Kenyatta University of Agriculture and Technology (JKUAT), Nairobi, Kenya P. O. Box 62000-00200, Nairobi. Kenya.
Open Vet J. 2012;2(1):58-64. Epub 2012 Jun 1.
Malaria parasites are known to mediate the induction of inflammatory immune responses at the maternal-foetal interface during placental malaria (PM) leading to adverse consequences like pre-term deliveries and abortions. Immunological events that take place within the malaria-infected placental micro-environment leading to retarded foetal growth and disruption of pregnancies are among the critical parameters that are still in need of further elucidation. The establishment of more animal models for studying placental malaria can provide novel ways of circumventing problems experienced during placental malaria research in humans such as inaccurate estimation of gestational ages. Using the newly established olive baboon (Papio anubis)-Plasmodium knowlesi (P. knowlesi) H strain model of placental malaria, experiments were carried out to determine placental cytokine profiles underlying the immunopathogenesis of placental malaria. Four pregnant olive baboons were infected with blood stage P. knowlesi H strain parasites on the one fiftieth day of gestation while four other uninfected pregnant olive baboons were maintained as uninfected controls. After nine days of infection, placentas were extracted from all the eight baboons through cesarean surgery and used for the processing of placental plasma and sera samples for cytokine sandwich enzyme linked immunosorbent assays (ELISA). Results indicated that the occurrence of placental malaria was associated with elevated concentrations of tumour necrosis factor alpha (TNF-α) and interleukin 12 (IL-12). Increased levels of IL-4, IL-6 and IL-10 and interferon gamma (IFN-γ) levels were detected in uninfected placentas. These findings match previous reports regarding immunity during PM thereby demonstrating the reliability of the olive baboon-P. knowlesi model for use in further studies.
众所周知,疟原虫在胎盘疟疾(PM)期间介导母胎界面处炎症免疫反应的诱导,导致早产和流产等不良后果。在受疟疾感染的胎盘微环境中发生的导致胎儿生长迟缓及妊娠中断的免疫事件,是仍需进一步阐明的关键参数之一。建立更多用于研究胎盘疟疾的动物模型,可以提供新方法来规避人类胎盘疟疾研究中遇到的问题,比如孕周估算不准确。利用新建立的橄榄狒狒(埃及狒狒)-诺氏疟原虫(诺氏疟原虫)H株胎盘疟疾模型,开展实验以确定胎盘疟疾免疫发病机制背后的胎盘细胞因子谱。4只怀孕的橄榄狒狒在妊娠第50天感染血期诺氏疟原虫H株寄生虫,另外4只未感染的怀孕橄榄狒狒作为未感染对照。感染9天后,通过剖宫产手术从所有8只狒狒身上取出胎盘,用于处理胎盘血浆和血清样本,进行细胞因子夹心酶联免疫吸附测定(ELISA)。结果表明,胎盘疟疾的发生与肿瘤坏死因子α(TNF-α)和白细胞介素12(IL-12)浓度升高有关。在未感染的胎盘中检测到IL-4、IL-6和IL-10水平以及干扰素γ(IFN-γ)水平升高。这些发现与之前关于胎盘疟疾期间免疫的报道相符,从而证明了橄榄狒狒-诺氏疟原虫模型用于进一步研究的可靠性。