ArticleFrontiers in pharmacology2018
Brain Lipopolysaccharide Preconditioning-Induced Gene Reprogramming Mediates a Tolerance State in Electroconvulsive Shock Model of Epilepsy.
Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Gut-microbiota-brain Axis and post-traumatic epilepsy.Epilepsia open · 2024Article
- Neuroinflammation mechanisms of neuromodulation therapies for anxiety and depression.Translational psychiatry · 2023Review
- Innate immune stimulation by monophosphoryl lipid A prevents chronic social defeat stress-induced anxiety-like behaviors in mice.Journal of neuroinflammation · 2022Article
- Dynamic Interleukin-1 Receptor Type 1 Signaling Mediates Microglia-Vasculature Interactions Following Repeated Systemic LPS.Journal of inflammation research · 2022Article
- Low-dose lipopolysaccharide as an immune regulator for homeostasis maintenance in the central nervous system through transformation to neuroprotective microglia.Neural regeneration research · 2021Review
- Pseudomonas aeruginosa outer membrane vesicles ameliorates lung ischemia-reperfusion injury by regulating the balance of regulatory T cells and Th17 cells through Tim-3 and TLR4/NF-κB pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
- Article
- The innate immune system and neurogenesis as modulating mechanisms of electroconvulsive therapy in pre-clinical studies.Journal of psychopharmacology (Oxford, England) · 2020Review
- Pilocarpine Induced Behavioral and Biochemical Alterations in Chronic Seizure-Like Condition in Adult Zebrafish.International journal of molecular sciences · 2020Article
- Anti-High Mobility Group Box-1 Monoclonal Antibody Attenuates Seizure-Induced Cognitive Decline by Suppressing Neuroinflammation in an Adult Zebrafish Model.Frontiers in pharmacology · 2020Article
- Immune Challenges and Seizures: How Do Early Life Insults Influence Epileptogenesis?Frontiers in pharmacology · 2020Review
- Mitochondrial Complex I Is an Essential Player in LPS-Induced Preconditioning in Differentiated PC12 Cells.Iranian journal of pharmaceutical research : IJPR · 2019Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is increasing evidence pointing toward the role of inflammatory processes in epileptic seizures, and reciprocally, prolonged seizures induce more inflammation in the brain. In this regard, effective strategies to control epilepsy resulting from neuroinflammation could be targeted. Based on the available data, preconditioning (PC) with low dose lipopolysaccharide (LPS) through the regulation of the TLR4 signaling pathway provides neuroprotection against subsequent challenge with injury in the brain. To test this, we examined the effects of a single and chronic brain LPS PC, which is expected to lead to reduction of inflammation against epileptic seizures induced by electroconvulsive shock (ECS). A total of 60 male Sprague Dawley rats were randomly assigned to five groups: control, vehicle (single and chronic), and LPS PC (single and chronic). We first recorded the data regarding the behavioral and histological changes. We further investigated the alterations of gene and protein expression of important mediators in relation to TLR4 and inflammatory signaling pathways. Interestingly, significant increased presence of NFκB inhibitors [Src homology 2-containing inositol phosphatase-1 (SHIP1) and Toll interacting protein (TOLLIP)] was observed in LPS-preconditioned animals. This result was also associated with over-expression of IRF3 activity and anti-inflammatory markers, along with down-regulation of pro-inflammatory mediators. Summarizing, the analysis revealed that PC with LPS prior to seizure induction may have a neuroprotective effect possibly by reprogramming the signaling response to injury.
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