ArticlePLoS pathogens2007
Edema toxin impairs anthracidal phospholipase A2 expression by alveolar macrophages.
Article in PLoS pathogens, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed.
- Early Circulating Edema Factor in Inhalational Anthrax Infection: Does It Matter?Microorganisms · 2024Article
- Modulation of Airway Expression of the Host Bactericidal Enzyme, sPLA2-IIA, by Bacterial Toxins.Toxins · 2023Review
- Bioactive lipid-based therapeutic approach to COVID-19 and other similar infections.Archives of medical science : AMS · 2023Article
- The interaction of secreted phospholipase A2-IIA with the microbiota alters its lipidome and promotes inflammation.JCI insight · 2022Article
- "Cell Membrane Theory of Senescence" and the Role of Bioactive Lipids in Aging, and Aging Associated Diseases and Their Therapeutic Implications.Biomolecules · 2021Review
- Article
- Very Early Blood Diffusion of the Active Lethal and Edema Factors of Bacillus anthracis After Intranasal Infection.The Journal of infectious diseases · 2020Article
- Article
- A transcriptomic snapshot of early molecular communication between Pasteuria penetrans and Meloidogyne incognita.BMC genomics · 2018Article
- Streptococcal Lancefield polysaccharides are critical cell wall determinants for human Group IIA secreted phospholipase A2 to exert its bactericidal effects.PLoS pathogens · 2018Article
- Arachidonic acid and other unsaturated fatty acids and some of their metabolites function as endogenous antimicrobial molecules: A review.Journal of advanced research · 2018Review
- In vivo dynamics of active edema and lethal factors during anthrax.Scientific reports · 2016Article
- The Roles of the Secreted Phospholipase AAdvances in immunology · 2016Review
- A new era of secreted phospholipase A₂.Journal of lipid research · 2015Article
- Crossing of the epithelial barriers by Bacillus anthracis: the Known and the Unknown.Frontiers in microbiology · 2015Review
- Review
- Cellular and physiological effects of anthrax exotoxin and its relevance to disease.Frontiers in cellular and infection microbiology · 2012Review
- Glycogen synthase kinase 3 activation is important for anthrax edema toxin-induced dendritic cell maturation and anthrax toxin receptor 2 expression in macrophages.Infection and immunity · 2011Article
- Adenomatous polyposis coli protein associates with C/EBP beta and increases Bacillus anthracis edema toxin-stimulated gene expression in macrophages.The Journal of biological chemistry · 2011Article
- Resistance of human alveolar macrophages to Bacillus anthracis lethal toxin.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacillus anthracis, the etiological agent of anthrax, is a spore-forming gram-positive bacterium. Infection with this pathogen results in multisystem dysfunction and death. The pathogenicity of B. anthracis is due to the production of virulence factors, including edema toxin (ET). Recently, we established the protective role of type-IIA secreted phospholipase A2 (sPLA2-IIA) against B. anthracis. A component of innate immunity produced by alveolar macrophages (AMs), sPLA2-IIA is found in human and animal bronchoalveolar lavages at sufficient levels to kill B. anthracis. However, pulmonary anthrax is almost always fatal, suggesting the potential impairment of sPLA2-IIA synthesis and/or action by B. anthracis factors. We investigated the effect of purified ET and ET-deficient B. anthracis strains on sPLA2-IIA expression in primary guinea pig AMs. We report that ET inhibits sPLA2-IIA expression in AMs at the transcriptional level via a cAMP/protein kinase A-dependent process. Moreover, we show that live B. anthracis strains expressing functional ET inhibit sPLA2-IIA expression, whereas ET-deficient strains induced this expression. This stimulatory effect, mediated partly by the cell wall peptidoglycan, can be counterbalanced by ET. We conclude that B. anthracis down-regulates sPLA2-IIA expression in AMs through a process involving ET. Our study, therefore, describes a new molecular mechanism implemented by B. anthracis to escape innate host defense. These pioneering data will provide new molecular targets for future intervention against this deadly pathogen.
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.