ArticleThe Journal of experimental medicine1993
Pore-forming bacterial toxins potently induce release of nitric oxide in porcine endothelial cells.
Article in The Journal of experimental medicine, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 73 citations in OpenAlex.
- Exploring the Role ofToxins · 2022Review
- Efficacy of Active Immunization With Attenuated α-Hemolysin and Panton-Valentine Leukocidin in a Rabbit Model of Staphylococcus aureus Necrotizing Pneumonia.The Journal of infectious diseases · 2020Article
- Review
- A potential key role for alpha-haemolysin ofBone & joint research · 2018Article
- Review
- The psmα locus regulates production of Staphylococcus aureus alpha-toxin during infection.Infection and immunity · 2014Article
- Dynamics of pulmonary endothelial barrier function in acute inflammation: mechanisms and therapeutic perspectives.Cell and tissue research · 2014Review
- Review
- Host response signature to Staphylococcus aureus alpha-hemolysin implicates pulmonary Th17 response.Infection and immunity · 2012Article
- The response of the host microcirculation to bacterial sepsis: does the pathogen matter?Journal of molecular medicine (Berlin, Germany) · 2010Review
- Staphylococcus aureus alpha-hemolysin activates the NLRP3-inflammasome in human and mouse monocytic cells.PloS one · 2009Article
- Interferons increase cell resistance to Staphylococcal alpha-toxin.Infection and immunity · 2008Article
- Perturbation of endothelial junction proteins by Staphylococcus aureus alpha-toxin: inhibition of endothelial gap formation by adrenomedullin.Histochemistry and cell biology · 2006Article
- Human endothelial cell activation and mediator release in response to Listeria monocytogenes virulence factors.Infection and immunity · 2001Article
- Alpha-toxin and gamma-toxin jointly promote Staphylococcus aureus virulence in murine septic arthritis.Infection and immunity · 1999Article
- Acylation of Escherichia coli hemolysin: a unique protein lipidation mechanism underlying toxin function.Microbiology and molecular biology reviews : MMBR · 1998Review
- Respiratory activity is essential for post-exponential-phase production of type 5 capsular polysaccharide by Staphylococcus aureus.Infection and immunity · 1996Article
- Pasteurella haemolytica leukotoxin induces bovine leukocytes to undergo morphologic changes consistent with apoptosis in vitro.Infection and immunity · 1996Article
- Bacterial modulins: a novel class of virulence factors which cause host tissue pathology by inducing cytokine synthesis.Microbiological reviews · 1996Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) is believed to play an important role in sepsis-related hypotension. We examined the effects of two pore-forming bacterial exotoxins, Escherichia coli hemolysin and Staphylococcus aureus alpha-toxin, on NO formation in cultured porcine pulmonary artery endothelial cells. NO was quantified using a difference-spectrophotometric method based on the rapid and stoichiometric reaction of NO with oxyhemoglobin. Endothelial cyclic guanosine monophosphate levels were also monitored. Both exotoxins increased NO synthesis in endothelial cells in a time- and dose-dependent manner to an extent exceeding that observed with the ionophore A23187 or thrombin. The capacity of exotoxins to induce NO formation may be relevant in patients with severe local or systemic bacterial infections.
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.