ReviewOxidative medicine and cellular longevity2013
Role of oxidative stress in the pathophysiology of pneumococcal meningitis.
Review in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- Melatonin Exerts Neuroprotective Effects in Escherichia coli/Lipopolysaccharide Induced Neuronal Injury via Regulating TFRC-Related Ferroptosis.Neurochemical research · 2026Article
- Roles of TIR domain-containing adaptor protein in tumor: Inflammation and immune regulation via toll-like receptor signaling.The Journal of international medical research · 2026Review
- The meninges as a neuroimmune interface: structure, barriers and roles in CNS disease.Fluids and barriers of the CNS · 2026Review
- Article
- Clinical features and risk factors of neonatal late-onset sepsis complicated by purulent meningitis.Frontiers in pediatrics · 2026Article
- Macrophage IL-1β turns meningeal fibroblasts into inflammatory amplifiers in pneumococcal infection.Frontiers in immunology · 2026Article
- [Therapeutic effects of inulin-type oligosaccharides ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Understanding the mechanisms ofTissue barriers · 2025Review
- Molecular mechanisms of streptococcal disruption of the blood-brain barrier and their pathogenic role in bacterial meningitis.Frontiers in immunology · 2025Review
- Review
- Integrating DNA/RNA microbe detection and host response for accurate diagnosis, treatment and prognosis of childhood infectious meningitis and encephalitis.Journal of translational medicine · 2024Article
- NLRP3 Activation Contributes to Memory Impairment in an Experimental Model of Pneumococcal Meningitis.Molecular neurobiology · 2024Article
- Addition of daptomycin for the treatment of pneumococcal meningitis: protocol for the AddaMAP study.BMJ open · 2023Article
- High Concentration of Protein Oxidation Biomarker O-Tyr/Phe Predicts Better Outcome in Childhood Bacterial Meningitis.Antioxidants (Basel, Switzerland) · 2023Article
- The oxidative stress response ofFrontiers in microbiology · 2023Review
- Article
- Association of Oxidative Stress with Neurological Disorders.Current neuropharmacology · 2022Article
- Reactive oxygen species and nitric oxide as mediators in plant hypersensitive response and stomatal closure.Plant signaling & behavior · 2021Article
- The Potentials of Melatonin in the Prevention and Treatment of Bacterial Meningitis Disease.Molecules (Basel, Switzerland) · 2021Review
- The blood-brain barrier dysfunction in sepsis.Tissue barriers · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pneumococcal meningitis is a life-threatening disease characterized by an acute purulent infection affecting the pia mater, the arachnoid, and the subarachnoid spaces. Streptococcus pneumoniae crosses the blood-brain barrier (BBB) by both transcellular traversal and disruption of the intraepithelial tight junctions to allow intercellular traversal. During multiplication, pneumococci release their bacterial products, which are highly immunogenic and may lead to an increased inflammatory response in the host. Thus, these compounds are recognized by antigen-presenting cells through the binding of toll-like receptors. These receptors induce the activation of myeloid differentiation factor 88 (MyD88), which interacts with various protein kinases, including IL-1 receptor-associated kinase-4 (IRAK4), which is phosphorylated and dissociated from MyD88. These products also interact with tumor necrosis factor receptor-associated factor 6 dependent signaling pathway (TRAF6). This cascade provides a link to NF- κ B-inducing kinase, resulting in the nuclear translocation of NF- κ B leading to the production of cytokines, chemokines, and other proinflammatory molecules in response to bacterial stimuli. Consequently, polymorphonuclear cells are attracted from the bloodstream and then activated, releasing large amounts of NO(•), O2(•), and H2O2. This formation generates oxidative and nitrosative stress, subsequently, lipid peroxidation, mitochondrial damage, and BBB breakdown, which contributes to cell injury during pneumococcal meningitis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.