Graduate Program in Animal Science, Universidade do Estado de Santa Catarina, Chapecó, Santa Catarina, Brazil.
Department of Microbiology and Parasitology, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.
Microb Pathog. 2018 Nov;124:284-290. doi: 10.1016/j.micpath.2018.08.044. Epub 2018 Aug 22.
Several evidences have suggested the involvement of enzymes belonging to the phosphotransfer network, formed by creatine kinase (CK), pyruvate kinase (PK) and adenylate kinase (AK), as well the oxidative stress on the pathogenesis of infectious diseases associated with the central nervous system (CNS). Thus, the aim of this study was to evaluate whether listeriosis alters the brain energy metabolism and/or causes oxidative stress in different brain structures of cattle experimentally infected by Listeria monocytogenes. The cytosolic CK activity was inhibited in the cerebral cortex, cerebellum, brainstem and hippocampus of infected animals compared to uninfected animals, while the mitochondrial CK activity was increased. The PK activity was inhibited in all brain structures of infected animals, while the AK activity was unchanged. Na, K-ATPase activity decreased in the cerebral cortex, cerebellum and hippocampus of animals infected by L. monocytogenes. Regarding the oxidative strees variables, the cerebellum and brainstem of infected animals showed increased thiobarbituric acid reactive substances, while the catalase activity was inhibited. Glutathione S-transferarase was inhibited in the cerebral cortex and brainstem of infected animals, and it was increased in the cerebellum. L. monocytogenes was quantified in the liver (n = 5/5) and cerebral cortex (n = 4/5) of the infected cattle. Based on these evidences, the nucleocytoplasmic communication between CK isoenzymes was insufficient to avoid an impairment of cerebral bioenergetics. Moreover, the inhibition on brain PK activity caused an impairment in the communication between sites of ATP generation and ATP utilization. The lipid peroxidation and alteration on antioxidant status observed in some brain structures were also involved during the disease. In summary, these alterations contribute to disease pathogenesis linked to CNS during cattle listeriosis.
已有多项证据表明，磷酸转移网络中的酶（包括肌酸激酶（CK）、丙酮酸激酶（PK）和腺苷酸激酶（AK））以及中枢神经系统（CNS）相关感染性疾病的氧化应激与疾病的发病机制有关。因此，本研究旨在评估李斯特菌感染是否会改变牛的脑能量代谢并/或在感染李斯特菌单核细胞增生李斯特菌的牛的不同脑结构中引起氧化应激。与未感染动物相比，感染动物的大脑皮质、小脑、脑干和海马中的细胞溶质 CK 活性受到抑制，而线粒体 CK 活性增加。PK 活性在感染动物的所有脑结构中均受到抑制，而 AK 活性不变。Na、K-ATPase 活性在感染动物的大脑皮质、小脑和海马中降低。关于氧化应激变量，感染动物的小脑和脑干中丙二醛反应物质增加，而过氧化氢酶活性受到抑制。感染动物的大脑皮质和脑干中的谷胱甘肽 S-转移酶受到抑制，而小脑中的谷胱甘肽 S-转移酶增加。在感染牛的肝脏（n=5/5）和大脑皮质（n=4/5）中定量检测到李斯特菌。基于这些证据，CK 同工酶的核质通讯不足以避免大脑生物能量的损伤。此外，脑 PK 活性的抑制导致 ATP 生成和利用部位之间的通讯受损。在一些脑结构中观察到的脂质过氧化和抗氧化状态改变也与疾病有关。综上所述，这些改变有助于牛李斯特菌病与 CNS 相关的发病机制。
