Dincel Gungor Cagdas, Atmaca Hasan Tarik, El-Ashram Saeed
Department of Medical Pathology, Faculty of Medicine, Ankara Medipol University, Ankara 06050, Turkey.
College of Life Science and Engineering, Foshan University, 18 Jiangwan Street, Foshan 528231, China.
Brain Sci. 2024 Dec 23;14(12):1298. doi: 10.3390/brainsci14121298.
(), an obligate food-borne intracellular parasite, causes severe neuropathology by establishing a persistent infection in the host brain. We have previously shown that infection induces severe neuropathology in the brain manifested by increased nitric oxide production, oxidative stress, glial activation/BBB damage, increased pro-inflammatory cytokine glia maturation factor-beta and induced apoptosis. The aim of this experimental study was to investigate the serum amyloid P (SAP) components, nuclear factor kappa B (NF-κB), interleukin-1 beta (IL-1β), caspase 1 (Casp 1), tumor necrosis factor-alpha (TNF-α) and complement 3 (C3) gene expressions on the 10th, 20th and 30th days after infection with in the neuroimmunopathogenesis of toxoplasmic encephalitis (TE) in mouse brains by real-time quantitative polymerase chain reaction. The study also aimed to determine whether there was a correlation between the markers included in the study on these critical days, which had not previously been investigated. The mRNA expression levels of SAP components, NF-κB, IL-1β, Casp 1, TNF-α and C3 were examined. The most notable outcome of this investigation was the observation that SAP components exhibited a 13.9-fold increase on day 10 post-infection, followed by a rapid decline in the subsequent periods. In addition, IL-1β expression increased 20-fold, while SAP components decreased 13-fold on day 20 after infection. Additionally, the TNF-α, Casp 1 and NF-κB expression levels were consistently elevated to above normal levels at each time point. This study identified SAP components, NF-κB, IL-1β, Casp 1 and TNF-α expressions as playing critical roles in TE neuroimmunopathogenesis. Furthermore, to the best of our knowledge, this is the first study to investigate SAP components during the transition from acute systemic infection to early/medium chronic and chronic infection and to explore the relationship between SAP components and other nuclear factors/pro-cytokines.
（）是一种专性食源性细胞内寄生虫，通过在宿主大脑中建立持续感染导致严重的神经病理学变化。我们之前已经表明，感染会在大脑中诱发严重的神经病理学变化，表现为一氧化氮生成增加、氧化应激、神经胶质细胞活化/血脑屏障损伤、促炎细胞因子胶质细胞成熟因子-β增加以及诱导细胞凋亡。本实验研究的目的是通过实时定量聚合酶链反应，研究小鼠脑弓形虫性脑炎（TE）神经免疫发病机制中，感染后第10天、20天和30天血清淀粉样蛋白P（SAP）成分、核因子κB（NF-κB）、白细胞介素-1β（IL-1β）、半胱天冬酶1（Casp 1）、肿瘤坏死因子-α（TNF-α）和补体3（C3）的基因表达。该研究还旨在确定在这些关键日子里所研究的标志物之间是否存在相关性，此前尚未对此进行过研究。检测了SAP成分、NF-κB、IL-1β、Casp 1。
