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利用从肯尼亚鸡中分离出的[病原体名称未给出]建立弓形虫病神经学小鼠模型。 (注:原文中“Using Isolated from Chicken in Kenya”部分似乎不完整,缺少具体被分离的东西,以上是根据现有内容尽量合理翻译)

Development of Neurological Mouse Model for Toxoplasmosis Using Isolated from Chicken in Kenya.

作者信息

Mokua Mose John, Muchina Kamau David, Kagira John Maina, Maina Naomi, Ngotho Maina, Njuguna Adele, Karanja Simon Muturi

机构信息

Department of Medical Laboratory Science, School of Medicine and Health Sciences, Kenya Methodist University, P.O. Box 45240-00100, Nairobi, Kenya.

Department of Public Health, Jomo Kenyatta University of Agriculture and Technology (JKUAT), P.O. Box 62000-00200, Nairobi, Kenya.

出版信息

Patholog Res Int. 2017;2017:4302459. doi: 10.1155/2017/4302459. Epub 2017 May 24.

Abstract

Animal models for the toxoplasmosis are scarce and have limitations. In this study, a neurological mouse model was developed in BALB/c mice infected intraperitoneally with 15 cysts of a isolate. The mice were monitored for 42 days and euthanized at different time points. Another group of mice were orally treated with dexamethasone (DXM: 2.66 mg/kg daily, 5.32 mg/kg daily) at 42 days after infection and monitored for a further 42 days. A mortality rate of 15% and 28.6% was observed in mice given 2.66 mg/kg/day and 5.32 mg/kg/day of DXM, respectively. The mean cyst numbers in the brain of DXM treated mice increased up to twofold compared with chronically infected untreated mice. Infections up to 42 days were associated with an increase in both IgM and IgG levels but following dexamethasone treatment, IgM levels declined but IgG levels continued on rising. The brain of toxoplasmosis infected mice showed mononuclear cellular infiltrations, neuronal necrosis, and cuffing. The severity of pathology was higher in mice treated with dexamethasone compared to the positive control groups. The findings of this study demonstrate that DXM-induced reactivation of chronic toxoplasmosis may be a useful development of laboratory animal model in outbred mice used for studies.

摘要

弓形虫病的动物模型稀缺且存在局限性。在本研究中,用15个某分离株的包囊经腹腔感染BALB/c小鼠,建立了一种神经学小鼠模型。对小鼠监测42天,并在不同时间点实施安乐死。另一组小鼠在感染后42天口服地塞米松(DXM:每日2.66毫克/千克,每日5.32毫克/千克),并进一步监测42天。给予2.66毫克/千克/天和5.32毫克/千克/天DXM的小鼠死亡率分别为15%和28.6%。与未经治疗的慢性感染小鼠相比,接受DXM治疗的小鼠脑内平均包囊数增加了两倍。感染长达42天时,IgM和IgG水平均升高,但地塞米松治疗后,IgM水平下降,而IgG水平继续上升。弓形虫病感染小鼠的脑显示单核细胞浸润、神经元坏死和血管套。与阳性对照组相比,地塞米松治疗的小鼠病理学严重程度更高。本研究结果表明,DXM诱导的慢性弓形虫病再激活可能是用于研究的远交系小鼠实验室动物模型的一个有益进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5724/5463144/71f7e309d0c3/PRI2017-4302459.001.jpg

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