ArticleImmunology2008
Effects of complement regulators bound to Escherichia coli K1 and Group B Streptococcus on the interaction with host cells.
Article in Immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Complement deficiency and neonatal immunity: a serum-limited, context-dependent framework.Pediatric research · 2026Review
- Intrinsic Maturational Neonatal Immune Deficiencies and Susceptibility to Group B Streptococcus Infection.Clinical microbiology reviews · 2017Review
- Review
- Listeria monocytogenes triggers the cell surface expression of Gp96 protein and interacts with its N terminus to support cellular infection.The Journal of biological chemistry · 2012Article
- The rickettsial OmpB β-peptide of Rickettsia conorii is sufficient to facilitate factor H-mediated serum resistance.Infection and immunity · 2012Article
- gp96 expression in neutrophils is critical for the onset of Escherichia coli K1 (RS218) meningitis.Nature communications · 2011Article
- Complement-mediated bactericidal activity of anti-factor H binding protein monoclonal antibodies against the meningococcus relies upon blocking factor H binding.Infection and immunity · 2011Article
- Different factor H-related protein patterns in siblings with typical hemolytic uremic syndrome.Pediatric nephrology (Berlin, Germany) · 2011Article
- Interactions of complement proteins C1q and factor H with lipid A and Escherichia coli: further evidence that factor H regulates the classical complement pathway.Protein & cell · 2011Article
- Deciphering the roles of outer membrane protein A extracellular loops in the pathogenesis of Escherichia coli K1 meningitis.The Journal of biological chemistry · 2011Article
- Extracellular loops of the Eschericia coli outer membrane protein A contribute to the pathogenesis of meningitis.The Journal of infectious diseases · 2011Article
- Fcγ receptor I alpha chain (CD64) expression in macrophages is critical for the onset of meningitis by Escherichia coli K1.PLoS pathogens · 2010Article
- IL-10 administration reduces PGE-2 levels and promotes CR3-mediated clearance of Escherichia coli K1 by phagocytes in meningitis.The Journal of experimental medicine · 2010Article
- Population structure of gut Escherichia coli and its role in development of extra-intestinal infections.Iranian journal of microbiology · 2010Article
- Nitric oxide/cGMP signalling induces Escherichia coli K1 receptor expression and modulates the permeability in human brain endothelial cell monolayers during invasion.Cellular microbiology · 2010Article
- Acquisition of factor H by a novel surface protein on group B Streptococcus promotes complement degradation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009Article
- Brain damage in newborn rat model of meningitis by Enterobacter sakazakii: a role for outer membrane protein A.Laboratory investigation; a journal of technical methods and pathology · 2009Article
- Recent advances in understanding the molecular basis of group B Streptococcus virulence.Expert reviews in molecular medicine · 2008Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Escherichia coli K1 and Group B Streptococcus (GBS) are the most common bacteria that cause meningitis during the neonatal period. Complement, the first line of defence in the host, acts on these bacteria to opsonize with various components of complement for subsequent presentation to phagocytes. To counteract these opsonization effects, E. coli and GBS bind to the complement regulators C4 binding protein and Factor H, respectively. Nonetheless, the deposition of complement components on these two bacteria from neonatal serum and their effect on the host cell interaction is unclear. Here we demonstrated that the deposition of complement proteins from adult serum prevented the invasion of E. coli into human brain microvascular endothelial cells, whereas the invasion of GBS was enhanced. In contrast, treatment with cord serum had no effect on the invasion of both these bacteria. We also examined the effect of the deposited complement proteins on phagocytosis using THP-1 cells and THP-1 cells differentiated into macrophages. Escherichia coli treated with adult serum neither attached nor entered these cells, whereas GBS was phagocytosed and survived efficiently. We further demonstrate that the inhibitory effect of complement proteins is the result of the bound complement inhibitors C4b-binding protein, in the case of E. coli, and Factor H, in the case of GBS. Taken together, these results suggest that E. coli and GBS utilize contrasting mechanisms of complement-mediated interactions with their target cells for successful establishment of disease.
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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.