Elwakil Bassma H, Bakr Basant A, Aljeldah Mohammed M, Shehata Nourhan S, Shahin Yahya H, Olama Zakia A, Augustyniak Maria, Aboul-Soud Mourad A M, El Wakil Abeer
Department of Medical Laboratory Technology, Faculty of Applied Health Sciences Technology, Pharos University in Alexandria, Alexandria P.O. Box 21311, Egypt.
Department of Zoology, Faculty of Science, Alexandria University, Alexandria P.O. Box 21568, Egypt.
Pathogens. 2022 Aug 18;11(8):933. doi: 10.3390/pathogens11080933.
Meningitis caused by and has lately become a prevalent cause of the central nervous system (CNS) infection. Bacterial invasion into the subarachnoid space prompts the releasing mechanism of chemokines and pro-inflammatory cytokines. The present study aimed to compare and meningitis concerning the memory, pro-inflammatory mediators and brain histopathological changes at different time intervals in adult Albino rats. The animals were sacrificed at three time intervals comprising 5, 10 and 15 days after meningitis induction. Cerebrospinal fluid (CSF) culture, relative brain weights, complete blood analysis, biochemical markers, levels of cytokine, chemokine and brain-derived neurotrophic factor (BDNF), neurotransmitter acetylcholine esterase (AChE) activity, and the brain histopathology of the infected rats in comparison to those in the control group were assessed. There was a significant increase in the levels of pro-inflammatory cytokines and chemokines including TNF-α, IL-1β, IL-6 and AChE after 5 days of bacterial meningitis infection with both and . The histopathological analysis of the cerebral cortex in the meningitis model at different time intervals revealed abundant numbers of dilated and congested blood vessels with severe hemorrhage, cerebral infarct, intracellular and extracellular vacuoles, and gliosis. Fifteen days post infection, a significant reduction in the brain tissue weight was observed. The meningitis model employing exhibited more evident time-dependent severity compared to , which may advocate its validity as a simple and effective research model to study meningitis of the CNS. This model may be utilized for further investigation to ascertain the molecular and biological association between bacterial meningitis and the development of the pathophysiological hallmarks underlying Alzheimer's disease in preclinical and clinical setups. Clinical extrapolation based on studies employing animal disease models should be carefully interpreted.
由[细菌名称1]和[细菌名称2]引起的脑膜炎最近已成为中枢神经系统（CNS）感染的常见原因。细菌侵入蛛网膜下腔会促使趋化因子和促炎细胞因子的释放机制。本研究旨在比较成年白化大鼠在不同时间间隔下[细菌名称1]和[细菌名称2]脑膜炎在记忆、促炎介质和脑组织病理学变化方面的情况。在诱导脑膜炎后的5天、10天和15天这三个时间间隔处死动物。评估脑脊液（CSF）培养、相对脑重量、全血分析、生化标志物、细胞因子、趋化因子和脑源性神经营养因子（BDNF）水平、神经递质乙酰胆碱酯酶（AChE）活性，以及与对照组相比感染大鼠的脑组织病理学。在[细菌名称1]和[细菌名称2]引起的细菌性脑膜炎感染5天后，促炎细胞因子和趋化因子水平显著升高，包括肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）和AChE。不同时间间隔下[细菌名称1]脑膜炎模型的大脑皮质组织病理学分析显示，有大量扩张和充血的血管，伴有严重出血、脑梗死、细胞内和细胞外空泡以及胶质细胞增生。感染后15天，观察到脑组织重量显著减轻。与[细菌名称2]相比，采用[细菌名称1]的脑膜炎模型表现出更明显的时间依赖性严重程度，这可能支持其作为研究中枢神经系统脑膜炎的简单有效研究模型的有效性。该模型可用于进一步研究，以确定在临床前和临床环境中细菌性脑膜炎与阿尔茨海默病潜在病理生理特征发展之间的分子和生物学关联。基于动物疾病模型研究的临床推断应谨慎解读。
