ArticleInfection and immunity1996
Protease cleavage of iron-transferrin augments pyocyanin-mediated endothelial cell injury via promotion of hydroxyl radical formation.
Article in Infection and immunity, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- Dual inhibitors ofChemical science · 2024Article
- NosP Detection of Heme ModulatesBiochemistry · 2023Article
- Deficiency of α-1-antitrypsin influences systemic iron homeostasis.International journal of chronic obstructive pulmonary disease · 2013Article
- In vivo evidence of free radical generation in the mouse lung after exposure to Pseudomonas aeruginosa bacterium: an ESR spin-trapping investigation.Free radical research · 2012Article
- Novel inhibitors of the Pseudomonas aeruginosa virulence factor LasB: a potential therapeutic approach for the attenuation of virulence mechanisms in pseudomonal infection.Antimicrobial agents and chemotherapy · 2011Article
- The role of the cytoplasmic heme-binding protein (PhuS) of Pseudomonas aeruginosa in intracellular heme trafficking and iron homeostasis.The Journal of biological chemistry · 2009Article
- Liver sinusoidal endothelial cells and acute non-oxidative hepatic injury induced by Pseudomonas aeruginosa pyocyanin.International journal of experimental pathology · 2008Article
- Cleavage of human transferrin by Porphyromonas gingivalis gingipains promotes growth and formation of hydroxyl radicals.Infection and immunity · 2004Article
- Biochemical model for inflammation of the brain: the effect of iron and transferrin on monocytes and lipid peroxidation.Metabolic brain disease · 2004Article
- Functional analysis of genes for biosynthesis of pyocyanin and phenazine-1-carboxamide from Pseudomonas aeruginosa PAO1.Journal of bacteriology · 2001Article
- Biological effects of menadione photochemistry: effects of menadione on biological systems may not involve classical oxidant production.The Biochemical journal · 2000Article
- The Pseudomonas aeruginosa secretory product pyocyanin inactivates alpha1 protease inhibitor: implications for the pathogenesis of cystic fibrosis lung disease.Infection and immunity · 1999Article
- Iron metabolism in the lower respiratory tract.Thorax · 1998Review
- Use of model plant hosts to identify Pseudomonas aeruginosa virulence factors.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Augmentation of oxidant injury to human pulmonary epithelial cells by the Pseudomonas aeruginosa siderophore pyochelin.Infection and immunity · 1997Article
- Role of oxidants in microbial pathophysiology.Clinical microbiology reviews · 1997Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Although a number of bacterium- and host-derived factors have been suggested to contribute to the pathogenesis of Pseudomonas aeruginosa-associated tissue injury, the mechanism remains unclear. We have previously shown that protease modification of iron (Fe)-transferrin generates new iron chelates capable of catalyzing hydroxyl radical (.OH) formation from superoxide and hydrogen peroxide. The latter two oxidants are generated during redox cycling of another P. aeruginosa secretory product, pyocyanin. The lung is a major site of P. aeruginosa infection, with damage to local endothelial cells contributing to the pathogenesis of such infections. Endothelial cells are highly susceptible to oxidant-mediated injury. Therefore, we examined whether pseudomonas elastase-cleaved Fe-transferrin and pyocyanin synergistically enhance pulmonary artery endothelial cell injury via .OH formation. By measuring 51Cr release from cultured endothelial cell monolayers, pseudomonas elastase-cleaved Fe-transferrin significantly augmented cell injury resulting from cellular exposure to sublethal concentrations of pyocyanin. This enhancement in injury was not protease specific, as similar results were obtained with pyocyanin in combination with trypsin- or porcine pancreatic elastase-cleaved Fe-transferrin. The association of iron with the transferrin appeared to be necessary in this process. Supporting the involvement of .OH generation via the Haber-Weiss reaction in augmenting cell injury, catalase, dimethyl thiourea, superoxide dismutase, deferoxamine, and dimethyl sulfoxide significantly inhibited cell injury resulting from exposure to pyocyanin and protease-cleaved Fe-transferrin. Furthermore, spin trapping demonstrated the production of .OH in this cellular system. We conclude that .OH formation resulting from the interaction of protease-cleaved Fe-transferrin and endothelial cell redox cycling of pyocyanin may contribute to P. aeruginosa-associated tissue injury via endothelial cell injury.
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