ArticleFEMS immunology and medical microbiology2009
Anthrax infection inhibits the AKT signaling involved in the E-cadherin-mediated adhesion of lung epithelial cells.
Article in FEMS immunology and medical microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Goblet cell breakdown: transcriptomics reveals Acinetobacter baumannii early and robust inflammatory response in differentiated human bronchial epithelial cells.Journal of biomedical science · 2025Article
- The subversion of toll-like receptor signaling by bacterial and viral proteases during the development of infectious diseases.Molecular aspects of medicine · 2022Review
- Gene expression profiling of primary human type I alveolar epithelial cells exposed to Bacillus anthracis spores reveals induction of neutrophil and monocyte chemokines.Microbial pathogenesis · 2018Article
- Microbial Degradation of Cellular Kinases Impairs Innate Immune Signaling and Paracrine TNFα Responses.Scientific reports · 2016Article
- Reverse-Phase Microarray Analysis Reveals Novel Targets in Lymph Nodes of Bacillus anthracis Spore-Challenged Mice.PloS one · 2015Article
- Proteomic strategies for the discovery of novel diagnostic and therapeutic targets for infectious diseases.Pathogens and disease · 2014Review
- GSK3β and the control of infectious bacterial diseases.Trends in microbiology · 2014Review
- Article
- Anthrax lethal toxin induces acute diastolic dysfunction in rats through disruption of the phospholamban signaling network.International journal of cardiology · 2013Article
- Vector-mediated selective expression of lethal factor, a toxic element of Bacillus anthracis, damages A549 cells via inhibition of MAPK and AKT pathways.International journal of medical sciences · 2013Article
- Opposite regulation by PI3K/Akt and MAPK/ERK pathways of tissue factor expression, cell-associated procoagulant activity and invasiveness in MDA-MB-231 cells.Journal of hematology & oncology · 2012Article
- Review
- Targeting the inflammasome and adenosine type-3 receptors improves outcome of antibiotic therapy in murine anthrax.World journal of biological chemistry · 2011Article
- Bacillus anthracis protease InhA increases blood-brain barrier permeability and contributes to cerebral hemorrhages.PloS one · 2011Article
- Anthrolysin O and fermentation products mediate the toxicity of Bacillus anthracis to lung epithelial cells under microaerobic conditions.FEMS immunology and medical microbiology · 2011Article
- Francisella Subverts Innate Immune Signaling: Focus On PI3K/Akt.Frontiers in microbiology · 2011Article
- Reverse phase protein microarrays advance to use in clinical trials.Molecular oncology · 2010Review
- Protein microarrays and biomarkers of infectious disease.International journal of molecular sciences · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effect of anthrax infection on phosphoprotein signaling was studied in human small airway lung epithelial cells exposed to B. anthracis spores of the plasmidless dSterne strain in comparison with the Sterne strain containing the toxigenic plasmid (pXO1). The differential regulation of phosphorylation was found in the mitogen-activated protein kinase cascade (ERK, p38, and P90RSK), the PI3K cascade (AKT, GSK-3alpha/beta), and downstream in the case of the proapoptotic BAD and the transcription factor STAT3. Both strains stimulate phosphorylation of CREB and inhibit phosphorylation of 4E-BP1 required for activation of cap-dependent translation. Downregulation of the survival AKT phosphorylation by the Sterne strain inhibits the process of Ca(2+)-dependent homophilic interaction of E-cadherin (EC) upon formation or repair of cell-cell contacts. Both lethal and edema toxins produced by the Sterne strain inhibit the AKT phosphorylation induced during the EC-mediated signaling. Activity of ERK1/2 and p38 inhibitors indicates that inhibition of AKT phosphorylation takes place through the ERK1/2-PI3K crosstalk. In Sterne spore-challenged mice, a specific inhibitor of PI3K/AKT, wortmannin, accelerates the lethal outcome, and reduction of AKT phosphorylation in the circulating blood cells coincides with the death of animals. We conclude that the PI3K/AKT pathway controlling the integrity of epithelium plays an important survival role in anthrax infection.
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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.