ArticleInfection and immunity2010
Meningococcal porin PorB prevents cellular apoptosis in a toll-like receptor 2- and NF-kappaB-independent manner.
Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 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
18 citing papers in PubMed, 32 citations in OpenAlex.
- Effects of surface-exposed sialic acid and LOS outer core on the ability of native Neisseria meningitidis outer membrane vesicles (nOMVs) to induce cytokine expression and pyroptotic pathways in THP-1-derived macrophages.Scientific reports · 2025Article
- Targeting PANoptosis in Bacterial-Induced Inflammatory Diseases: Mechanisms and Therapeutic Interventions.Journal of inflammation research · 2025Review
- Gonococcal PorB: a multifaceted modulator of host immune responses.Trends in microbiology · 2024Review
- Article
- HrpA anchors meningococci to the dynein motor and affects the balance between apoptosis and pyroptosis.Journal of biomedical science · 2022Article
- Outer membrane vesicles from Neisseria gonorrhoeae target PorB to mitochondria and induce apoptosis.PLoS pathogens · 2018Article
- Outer Membrane Vesicles (OMVs) of Gram-negative Bacteria: A Perspective Update.Frontiers in microbiology · 2017Review
- Polyionic vaccine adjuvants: another look at aluminum salts and polyelectrolytes.Clinical and experimental vaccine research · 2015Review
- Disease-associated Neisseria meningitidis isolates inhibit wound repair in respiratory epithelial cells in a type IV pilus-independent manner.Infection and immunity · 2014Article
- Crystallographic analysis of Neisseria meningitidis PorB extracellular loops potentially implicated in TLR2 recognition.Journal of structural biology · 2014Article
- Structure-function studies of the Neisseria gonorrhoeae major outer membrane porin.Infection and immunity · 2013Article
- In vivo and in vitro characterization of the immune stimulating activity of the Neisserial porin PorB.PloS one · 2013Article
- Toll-like receptor 2-dependent activity of native major outer membrane protein proteosomes of Chlamydia trachomatis.Infection and immunity · 2013Article
- The amino acid sequence of Neisseria lactamica PorB surface-exposed loops influences Toll-like receptor 2-dependent cell activation.Infection and immunity · 2012Article
- Review: apoptotic mechanisms in bacterial infections of the central nervous system.Frontiers in immunology · 2012Article
- Bacterial outer membrane vesicles in disease and preventive medicine.Seminars in immunopathology · 2011Review
- Acute kidney injury in a mouse model of meningococcal disease.International journal of immunopathology and pharmacologyArticle
- Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Meningococcal porin PorB is an inhibitor of apoptosis induced via the intrinsic pathway in various cell types. This effect is attributed to prevention of mitochondrial depolarization and of subsequent release of proapoptotic mitochondrial factors. To determine whether apoptosis is globally inhibited by PorB, we compared the intrinsic and extrinsic pathways in HeLa cells. Interestingly, PorB does not prevent extrinsic apoptosis induced by tumor necrosis factor alpha plus cycloheximide, suggesting a unique mitochondrial pathway specificity. Several intracellular factors regulated by NF-kappaB, including members of the Bcl-2 family and of the inhibitor of apoptosis (IAP) family, play major roles in controlling apoptosis, and some of them are thought to contribute to the antiapoptotic effect of the gonococcal porin, PIB. However, most of the members of the Bcl-2 family and the IAP family are not induced by meningococcal PorB in HeLa cells, with the exception of Bfl-1/A1. Interestingly, PorB does not induce NF-kappaB activation in HeLa cells, likely due to a lack of Toll-like receptor 2 (TLR2) expression in these cells. Bfl-1/A1 expression is also regulated by CBF1, a nuclear component of the Notch signaling pathway, independent of NF-kappaB activation. Since HeLa cells are protected by PorB from intrinsic apoptosis events, regardless of TLR2 and NF-kappaB expression, the possibility of a contribution of alternative signaling pathways to this effect cannot be excluded. In this paper, we describe an initial dissection of the cascade of cellular events involved in the antiapoptotic effect of PorB in the absence of TLR2.
Indexed as
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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.