ArticleMediators of inflammation2016
Lack of Proinflammatory Cytokine Interleukin-6 or Tumor Necrosis Factor Receptor-1 Results in a Failure of the Innate Immune Response after Bacterial Meningitis.
Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
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- Gallic Acid Alleviates Injury of Intestine Induced by Escherichia Coli: Protective Role of Metalloproteinase and Antioxidants on Small Intestine In-vivo.Galen medical journal · 2024Article
- Peripheral white blood cell patterns in children with hydrocephalus as a response to ventriculo-peritoneal shunt infection.PloS one · 2024Article
- Anti-Inflammatory Effects of Marine Bioactive Compounds and Their Potential as Functional Food Ingredients in the Prevention and Treatment of Neuroinflammatory Disorders.Molecules (Basel, Switzerland) · 2022Review
- Autoimmunity, cancer and COVID-19 abnormally activate wound healing pathways: critical role of inflammation.Histochemistry and cell biology · 2022Review
- Pneumolysin boosts the neuroinflammatory response to Streptococcus pneumoniae through enhanced endocytosis.Nature communications · 2022Article
- Leukocyte cytokine responses in adult patients with mitochondrial DNA defects.Journal of molecular medicine (Berlin, Germany) · 2022Article
- In vivo tissue optical clearing assisted through-skull targeted photothrombotic ischemic stroke model in mice.Journal of biomedical optics · 2022Article
- The Immune Response in Adipocytes and Their Susceptibility to Infection: A Possible Relationship with Infectobesity.International journal of molecular sciences · 2022Review
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- The formyl peptide receptor agonist Ac2-26 alleviates neuroinflammation in a mouse model of pneumococcal meningitis.Journal of neuroinflammation · 2020Article
- Impact of different Streptococcus pneumoniae on the secretion of interleukin and adhesin from THP-1 monocytes.Journal of clinical laboratory analysis · 2019Article
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- Blood‒Brain Barrier Pathology and CNS Outcomes inInternational journal of molecular sciences · 2018Review
- Toll-Like Receptor 2-Mediated Glial Cell Activation in a Mouse Model of Cuprizone-Induced Demyelination.Molecular neurobiology · 2018Article
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- CRAMP deficiency leads to a pro-inflammatory phenotype and impaired phagocytosis after exposure to bacterial meningitis pathogens.Cell communication and signaling : CCS · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The most frequent pathogen that causes bacterial meningitis is the Gram-positive bacterium Streptococcus pneumoniae. By entering the brain, host cells will be activated and proinflammatory cytokines like interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) are released. The goal of the current study was to examine the interaction between IL-6 and TNFR1 as receptor for TNF-α and the innate immune response in vivo in a model of Streptococcus pneumoniae-induced meningitis. For the experiments IL-6(-/-), TNFR1(-/-), and TNFR1-IL-6(-/-) KO mice were used. Our results revealed higher mortality rates and bacterial burden after infection in TNFR1(-/-), IL-6(-/-), and TNFR1-IL-6(-/-) mice and a decreased immune response including lower neutrophil infiltration in the meninges of TNFR1(-/-) and TNFR1-IL-6(-/-) mice in contrast to IL-6(-/-) and wild type mice. Furthermore, the increased mortality of TNFR1(-/-) and TNFR1-IL-6(-/-) mice correlated with decreased glial cell activation compared to IL-6(-/-) or wild type mice after pneumococcal meningitis. Altogether, the results show the importance of TNFR1 and IL-6 in the regulation of the innate immune response. The lack of TNFR1 and IL-6 results in higher mortality by weakened immune defence, whereas the lack of TNFR1 results in more severe impairment of the innate immune response than the lack of IL-6 alone.
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Registered trials
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