ArticleInfection and immunity2004
Complement activation and complement-dependent inflammation by Neisseria meningitidis are independent of lipopolysaccharide.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 56 citations in OpenAlex.
- Comparative effects of early randomized immune or non-immune-enhancing enteral nutrition on cytokine production in children with septic shock.Intensive care medicine · 2005Trial
- Article
- Inhibition of the lectin pathway of complement activation reduces LPS-induced acute respiratory distress syndrome in mice.Frontiers in immunology · 2023Article
- Immune correlates of tuberculosis disease and risk translate across species.Science translational medicine · 2020Article
- P-selectin drives complement attack on endothelium during intravascular hemolysis in TLR-4/heme-dependent manner.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Human Endothelial Cell Activation by Escherichia coli and Staphylococcus aureus Is Mediated by TNF and IL-1β Secondarily to Activation of C5 and CD14 in Whole Blood.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Meningococcal disease and the complement system.Virulence · 2014Review
- Neutralization of Neisseria meningitidis outer membrane vesicles.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2011Article
- Ex vivo model of meningococcal bacteremia using human blood for measuring vaccine-induced serum passive protective activity.Clinical and vaccine immunology : CVI · 2009Article
- Stages of meningococcal sepsis simulated in vitro, with emphasis on complement and Toll-like receptor activation.Infection and immunity · 2008Article
- The alternative complement pathway revisited.Journal of cellular and molecular medicine · 2008Review
- Sensing gram-negative bacterial lipopolysaccharides: a human disease determinant?Infection and immunity · 2008Review
- Complement activation and cytokine response by BioProtein, a bacterial single cell protein.Clinical and experimental immunology · 2007Article
- MyD88-dependent signaling affects the development of meningococcal sepsis by nonlipooligosaccharide ligands.Infection and immunity · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fulminant meningococcal sepsis has been termed the prototypical lipopolysaccharide (LPS)-mediated gram-negative septic shock. Systemic inflammation by activated complement and cytokines is important in the pathogenesis of this disease. We investigated the involvement of meningococcal LPS in complement activation, complement-dependent inflammatory effects, and cytokine or chemokine production. Whole blood anticoagulated with lepirudin was stimulated with wild-type Neisseria meningitidis H44/76 (LPS+), LPS-deficient N. meningitidis H44/76lpxA (LPS-), or purified meningococcal LPS (NmLPS) at concentrations that were relevant to meningococcal sepsis. Complement activation products, chemokines, and cytokines were measured by enzyme-linked immunosorbent assays, and granulocyte CR3 (CD11b/CD18) upregulation and oxidative burst were measured by flow cytometry. The LPS+ and LPS- N. meningitidis strains both activated complement effectively and to comparable extents. Purified NmLPS, used at a concentration matched to the amount present in whole bacteria, did not induce any complement activation. Both CR3 upregulation and oxidative burst were also induced, independent of LPS. Interleukin-1beta (IL-1beta), tumor necrosis factor alpha, and macrophage inflammatory protein 1alpha production was predominantly dependent on LPS, in contrast to IL-8 production, which was also markedly induced by the LPS- meningococci. In this whole blood model of meningococcal sepsis, complement activation and the immediate complement-dependent inflammatory effects of CR3 upregulation and oxidative burst occurred independent of LPS.
Indexed as
Identifiers
What OpenQuestion holds
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.