Oxidative Stress, Cytokine/Chemokine and Disruption of Blood–Brain Barrier in Neonate Rats After Meningitis by Streptococcus agalactiae

Abstract

We verify the levels of cytokine/chemokine, myeloperoxidase activity, oxidative stress and disruption of BBB in hippocampus and cortex of the neonate Wistar rats after meningitis by S. agalactiae. In the hippocampus the levels were increased of CINC-1 at 6 h and 12 h, IL-1β at 6, 12 and 24 h, IL-6 at 6, 24 and 96 h, IL-10 at 24, 48 and 96 h and TNF-α at 24 h and 96 h. In the cortex the CINC-1 and IL-1β levels were found increased at 6 h. The MPO activity was significantly elevated at 24, 48 and 98 h in hippocampus and at 6, 12, 24, 48 and 96 h in the cortex. The breakdown of BBB started at 12 h.TBARS levels were elevated in the hippocampus at 6, 12, 24, 48, 72 and 96 h and cortex at 72 and 96 h. Protein carbonyls were elevated in the hippocampus and cortex at 6, 24, 48, 72 and 96 h. There was a decrease of SOD activity in hippocampus and in cortex. Catalase activity was elevated in hippocampus at 6 h and in the cortex at 12 and 96 h. Neonatal bacterial infections of the CNS are severe, the interference with the complex network of cytokines/chemokine, other inflammatory mediators and oxidants tend to aggravate the illness and can be involved in the breakdown of the BBB.

Exogenous Administration of PACAP Alleviates Traumatic Brain Injury in Rats through a Mechanism Involving the TLR4/MyD88/NF-κB Pathway

“…Prior work indicates that inflammatory mediators play an important role in the pathogenesis of experimental traumatic brain injury (Chen et al, 2008). For instance, TNF-a and IL-1b have been shown to affect the integrity of the blood-brain barrier, cerebral edema, and neuronal damage, and participate in the mechanisms of TBI (Barichello et al, 2011;Li et al, 2011;Lloyd et al, 2008). A number of studies have demonstrated that PACAP can modulate inflammatory factor production, including proinflammatory cytokines and ICAM-1, in vivo or in vitro (Armstrong et al, 2008;Arumugam et al, 2009;Reglodi et al, 2002).…”

Pathogens Penetrating the Central Nervous System: Infection Pathways and the Cellular and Molecular Mechanisms of Invasion

“…Group B streptococcus, S. pneumoniae, and S. suis invade brain microvascular endothelial cells via transcellular mechanisms; however, the associated production of proinflammatory cytokines, the activity of pore-forming toxins, and the induction of plasmin activity may also lead to a concurrent weakening of the BBB, potentially opening a paracellular route of entry. In vivo and in vitro studies have shown that group B streptococci, pneumococci, and S. suis induce the production of a range of cytokines and chemokines, including IL-1␤, IL-6, IL-8, IL-10, TNF-␣, macrophage chemoattractant protein 1 (MCP-1), granulocyte-macrophage colony-stimulating factor (GM-CSF), Gro-␣, and Gro-␤, in brain microvascular endothelial cells (109,(256)(257)(258)) and brain tissue (94,259,260). The stimulation of HBMECs with cytokines (including TNF-␣, IL-1␤, IL-6, and IL-17F) leads to cytoskeletal rearrangements and a redistribution of tight junction and adherens junction proteins, resulting in a decrease in barrier integrity (261)(262)(263)(264)(265)(266)(267).…”

Evaluation of the brain-derived neurotrophic factor, nerve growth factor and memory in adult rats survivors of the neonatal meningitis by Streptococcus agalactiae

“…This neurotrophin can protect axons, myelin from inflammatory injury and also can modulate the immune system, reducing the magnitude of the excitotoxicity during acute inflammatory activation (Colafrancesco and Villoslada, 2011). Previous study we shown that meningitis by GBS cause oxidative stress, increased of the cytokines/chemokine and BBB breakdown in the first hours after induction (Barichello et al, 2011), a follow up studies of children revealed that, more than ten years after recovery from bacterial meningitis, significant neurological and intellectual impairments still persist (Grimwood et al, 2000). These findings suggest that the meningitis model could be a good research tool for the study of the biological mechanisms involved in the behavioral alterations secondary to GBS meningitis.…”

“…Rats underwent a cisterna magna tap with a 23-gauge needle. The animals received either 10 L of sterile saline as a placebo or an equivalent volume of S. agalactiae suspension at a concentration of 1 × 10 6 cfu/mL and were subsequently returned to their cages (Barichello et al, 2011;Trampuz et al, 2007). Meningitis was documented by a quantitative culture of 5 L of CSF obtained by puncture of the cisterna magna (Barichello et al, 2010b).…”