TY - JOUR
T1 - Diabetes Exacerbates Sepsis-Induced Neuroinflammation and Brain Mitochondrial Dysfunction
AU - de Souza Stork, Solange
AU - Hübner, Marcos
AU - Biehl, Erica
AU - Danielski, Lucineia Gainski
AU - Bonfante, Sandra
AU - Joaquim, Larissa
AU - Denicol, Tais
AU - Cidreira, Thaina
AU - Pacheco, Anita
AU - Bagio, Erick
AU - Lanzzarin, Everton
AU - Bernades, Gabriela
AU - de Oliveira, Mariana Pacheco
AU - da Silva, Larissa Espindola
AU - Mack, Josiel M.
AU - Bobinski, Franciane
AU - Rezin, Gislaine Tezza
AU - Barichello, Tatiana
AU - Streck, Emilio Luiz
AU - Petronilho, Fabricia
N1 - Publisher Copyright:
© 2022, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
PY - 2022/12
Y1 - 2022/12
N2 - 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.
AB - 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.
KW - Diabetes
KW - Neuroinflammation
KW - Oxidative stress
KW - Sepsis
UR - http://www.scopus.com/inward/record.url?scp=85131677924&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85131677924&partnerID=8YFLogxK
U2 - 10.1007/s10753-022-01697-y
DO - 10.1007/s10753-022-01697-y
M3 - Article
C2 - 35689164
AN - SCOPUS:85131677924
SN - 0360-3997
VL - 45
SP - 2352
EP - 2367
JO - Inflammation
JF - Inflammation
IS - 6
ER -