ArticleInfection and immunity2008
Important role for Toll-like receptor 9 in host defense against meningococcal sepsis.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 51 citations in OpenAlex.
- PCR-positive meningococcal CSF infection without pleocytosis but high IL-6 and IL-8.Infection · 2024Article
- Vertebrate and Invertebrate Animal and New In Vitro Models for StudyingPathogens (Basel, Switzerland) · 2023Review
- Deciphering the TLR transcriptome and downstream signaling pathway in cerebrospinal fluid in pediatric meningitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Article
- Dendritic Cell-Specific Role for Pellino2 as a Mediator of TLR9 Signaling Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- DNA Sensing in the Innate Immune Response.Physiology (Bethesda, Md.) · 2020Review
- Molecular and Structural Basis of DNA Sensors in Antiviral Innate Immunity.Frontiers in immunology · 2020Review
- Cell Type Specific Expression of Toll-Like Receptors in Human Brains and Implications in Alzheimer's Disease.BioMed research international · 2019Review
- Article
- Article
- Review
- Toll-Like Receptor 9 Contributes to Defense against Acinetobacter baumannii Infection.Infection and immunity · 2015Article
- Genetic polymorphisms associated with the inflammatory response in bacterial meningitis.BMC medical genetics · 2015Article
- Cerebrospinal-fluid cytokine and chemokine profile in patients with pneumococcal and meningococcal meningitis.BMC infectious diseases · 2013Article
- Genetic variants in toll-like receptor 2 (TLR2), TLR4, TLR9, and FCγ receptor II are associated with antibody response to quadrivalent meningococcal conjugate vaccine in HIV-infected youth.Clinical and vaccine immunology : CVI · 2013Article
- Toll-like receptor 9 polymorphisms are associated with severity variables in a cohort of meningococcal meningitis survivors.BMC infectious diseases · 2012Article
- Burn injury triggered dysfunction in dendritic cell response to TLR9 activation and resulted in skewed T cell functions.PloS one · 2012Article
- Importance of Toll-like receptor 9 in host defense against M1T1 group A Streptococcus infections.Journal of innate immunity · 2012Article
- The Role of TLR2 in Infection and Immunity.Frontiers in immunology · 2012Article
- A nonsynonymous polymorphism of IRAK4 associated with increased prevalence of gram-positive infection and decreased response to toll-like receptor ligands.Journal of innate immunity · 2011Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neisseria meningitidis is a leading cause of meningitis and sepsis. The pathogenesis of meningococcal disease is determined by both bacterial virulence factors and the host inflammatory response. Toll-like receptors (TLRs) are prominent activators of the inflammatory response, and TLR2, -4, and -9 have been reported to be involved in the host response to N. meningitidis. While TLR4 has been suggested to play an important role in early containment of infection, the roles of TLR2 and TLR9 in meningococcal disease are not well described. Using a model for meningococcal sepsis, we report that TLR9(-/-) mice displayed reduced survival and elevated levels of bacteremia compared to wild-type mice. In contrast, TLR2(-/-) mice controlled the infection in a manner comparable to that of wild-type mice. TLR9 deficiency was also associated with reduced bactericidal activity in vitro, which was accompanied by reduced production of nitric oxide by TLR9-deficient macrophages. Interestingly, TLR9(-/-) mice recruited more macrophages to the bloodstream than wild-type mice and produced elevated levels of cytokines at late time points during infection. At the cellular level, activation of signal transduction and induction of cytokine gene expression were independent of TLR2 or TLR9 in macrophages and conventional dendritic cells. In contrast, plasmacytoid dendritic cells relied entirely on TLR9 to induce these activities. Thus, our data demonstrate an important role for TLR9 in host defense against N. meningitidis.
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Registered trials
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.