de Souza Stork Solange, Hübner Marcos, Biehl Erica, Danielski Lucineia Gainski, Bonfante Sandra, Joaquim Larissa, Denicol Tais, Cidreira Thaina, Pacheco Anita, Bagio Erick, Lanzzarin Everton, Bernades Gabriela, de Oliveira Mariana Pacheco, da Silva Larissa Espindola, Mack Josiel M, Bobinski Franciane, Rezin Gislaine Tezza, Barichello Tatiana, Streck Emilio Luiz, Petronilho Fabricia
Laboratory of Neurobiology of Inflammatory and Metabolic Processes, Health Sciences Unit, Graduate Program in Health Sciences, University of South Santa Catarina, Tubarão, SC, Brazil.
Laboratory of Experimental Neurology, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC), Criciúma, SC, Brazil.
Inflammation. 2022 Dec;45(6):2352-2367. doi: 10.1007/s10753-022-01697-y. Epub 2022 Jun 10.
Sepsis is a life-threatening organ dysfunction, which demands notable attention for its treatment, especially in view of the involvement of immunodepressed patients, as the case of patients with diabetes mellitus (DM), who constitute a population susceptible to develop infections. Thus, considering this endocrine pathology as an implicatory role on the immune system, the aim of this study was to show the relationship between this disease and sepsis on neuroinflammatory and neurochemical parameters. Levels of IL-6, IL-10, brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and mitochondrial respiratory chain complexes were evaluated in the hippocampus and prefrontal cortex 24 h after sepsis by cecal ligation and perforation (CLP) in Wistar rats induced to type 1 diabetes by alloxan (150 mg/kg). It was verified that diabetes implied immune function after 24 h of sepsis, since it contributed to the increase of the inflammatory process with higher production of IL-6 and decreased levels of IL-10 only in the hippocampus. In the same brain area, a several decrease in NGF level and activity of complexes I and II of the mitochondrial respiratory chain were observed. Thus, diabetes exacerbates neuroinflammation and results in mitochondrial impairment and downregulation of NGF level in the hippocampus after sepsis.
脓毒症是一种危及生命的器官功能障碍，其治疗需要特别关注，尤其是考虑到免疫抑制患者的情况，例如糖尿病（DM）患者，他们是易发生感染的人群。因此，鉴于这种内分泌病理对免疫系统的影响作用，本研究的目的是揭示这种疾病与脓毒症在神经炎症和神经化学参数方面的关系。通过用四氧嘧啶（150mg/kg）诱导Wistar大鼠患1型糖尿病，然后进行盲肠结扎和穿孔（CLP）诱导脓毒症，在脓毒症发生24小时后评估海马体和前额叶皮质中白细胞介素-6（IL-6）、白细胞介素-10（IL-10）、脑源性神经营养因子（BDNF）、神经生长因子（NGF）以及线粒体呼吸链复合物的水平。结果证实，脓毒症24小时后糖尿病影响了免疫功能，因为它导致炎症过程加剧，仅在海马体中IL-6产生增加而IL-10水平降低。在同一脑区，观察到NGF水平以及线粒体呼吸链复合物I和II的活性均有明显下降。因此，糖尿病会加剧脓毒症后的神经炎症，导致海马体中的线粒体损伤以及NGF水平下调。
