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无乳链球菌感染实验性感染的银鲶鱼后,会损害其大脑的生物能量。

Streptococcus agalactiae impairs cerebral bioenergetics in experimentally infected silver catfish.

机构信息

Department of Microbiology and Parasitology, Universidade Federal de Santa Maria (UFSM), Santa Maria, RS, Brazil.

Department of Physiology and Pharmacology, Universidade Federal de Santa Maria (UFSM), Santa Maria, RS, Brazil.

出版信息

Microb Pathog. 2017 Oct;111:28-32. doi: 10.1016/j.micpath.2017.08.013. Epub 2017 Aug 12.

Abstract

It is becoming evident that bacterial infectious diseases affect brain energy metabolism, where alterations of enzymatic complexes of the mitochondrial respiratory chain and creatine kinase (CK) lead to an impairment of cerebral bioenergetics which contribute to disease pathogenesis in the central nervous system (CNS). Based on this evidence, the aim of this study was to evaluate whether alterations in the activity of complex IV of the respiratory chain and CK contribute to impairment of cerebral bioenergetics during Streptococcus agalactiae infection in silver catfish (Rhamdia quelen). The activity of complex IV of the respiratory chain in brain increased, while the CK activity decreased in infected animals compared to uninfected animals. Brain histopathology revealed inflammatory demyelination, gliosis of the brain and intercellular edema in infected animals. Based on this evidence, S. agalactiae infection causes an impairment in cerebral bioenergetics through the augmentation of complex IV activity, which may be considered an adaptive response to maintain proper functioning of the electron respiratory chain, as well as to ensure ongoing electron flow through the electron transport chain. Moreover, inhibition of cerebral CK activity contributes to lower availability of ATP, contributing to impairment of cerebral energy homeostasis. In summary, these alterations contribute to disease pathogenesis linked to the CNS.

摘要

越来越明显的是,细菌性传染病会影响大脑的能量代谢,其中线粒体呼吸链和肌酸激酶(CK)的酶复合物的改变会导致大脑生物能量学的损害,从而导致中枢神经系统(CNS)疾病的发病机制。基于这一证据,本研究旨在评估链球菌感染对银鲶(Rhamdia quelen)大脑生物能量学的影响是否与呼吸链复合物 IV 和 CK 的活性改变有关。与未感染动物相比,感染动物大脑呼吸链复合物 IV 的活性增加,而 CK 活性降低。脑组织病理学显示,感染动物存在炎症性脱髓鞘、脑胶质增生和细胞间水肿。基于这一证据,链球菌感染通过增加复合物 IV 的活性导致大脑生物能量学受损,这可能被认为是一种适应性反应,以维持电子呼吸链的正常功能,并确保电子通过电子传递链持续流动。此外,大脑 CK 活性的抑制会导致 ATP 的可用性降低,从而导致大脑能量平衡受损。总之,这些改变与 CNS 相关的疾病发病机制有关。

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