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弓形虫感染通过细胞因子网络促进神经炎症并诱导BALB/c小鼠痛觉过敏。

Toxoplasma gondii Infection Promotes Neuroinflammation Through Cytokine Networks and Induced Hyperalgesia in BALB/c Mice.

作者信息

Mahmoudvand Hossein, Ziaali Naser, Ghazvini Hamed, Shojaee Saeideh, Keshavarz Hossein, Esmaeilpour Khadijeh, Sheibani Vahid

机构信息

Research Center for Tropical and Infectious Diseases, Kerman University of Medical Sciences, Kerman, Iran.

Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, Iran.

出版信息

Inflammation. 2016 Feb;39(1):405-412. doi: 10.1007/s10753-015-0262-6.

Abstract

We hypothesized that in Toxoplasma gondii infection, communication among immune cells promotes neuroinflammation through cytokine networks and induces pain sensitivity under conditions of neuropathic pain. The animal model of Toxoplasma infection was established by the intraperitoneal inoculation of 20-25 tissue cysts from Tehran strain of T. gondii to BALB/c mice. Amitriptyline (20 mg/kg, i.p., 1/day) administrated to animals for 7 days before behavioral tests. Pain behavioral tests including tail flick, hot plate, and formalin test were evaluated in all the groups. The mRNA levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 were examined by real-time PCR. Results revealed that T. gondii induce hyperalgesia in the infected mice, whereas amitriptyline showed a promising effect against the hyperalgesia induced by Toxoplasma infection. The mRNA levels of the aforementioned cytokines significantly (P < 0.05) increased in the infected mice compared to the uninfected ones. Obtained findings suggested that T. gondii infection could promote neuroinflammation through cytokine networks and induced hyperalgesia in BALB/c mice, whereas amitriptyline as an analgesic drug reverses them.

摘要

我们推测,在弓形虫感染中,免疫细胞之间的通讯通过细胞因子网络促进神经炎症,并在神经性疼痛的情况下诱导疼痛敏感性。通过向BALB/c小鼠腹腔接种来自德黑兰株弓形虫的20 - 25个组织包囊来建立弓形虫感染的动物模型。在行为测试前7天,给动物腹腔注射阿米替林(20 mg/kg,每天1次)。对所有组进行包括甩尾、热板和福尔马林测试在内的疼痛行为测试。通过实时PCR检测肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β和IL-6的mRNA水平。结果显示,弓形虫在感染小鼠中诱导痛觉过敏,而阿米替林对弓形虫感染诱导的痛觉过敏显示出有前景的效果。与未感染小鼠相比,感染小鼠中上述细胞因子的mRNA水平显著(P < 0.05)升高。所得结果表明,弓形虫感染可通过细胞因子网络促进神经炎症,并在BALB/c小鼠中诱导痛觉过敏,而作为镇痛药的阿米替林可逆转这些情况。

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