ArticleInfection and immunity1999
The Pseudomonas aeruginosa secretory product pyocyanin inactivates alpha1 protease inhibitor: implications for the pathogenesis of cystic fibrosis lung disease.
Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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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.
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Who cites it
35 citing papers in PubMed, 72 citations in OpenAlex.
- Natural products shape microbial ecology and disease in the cystic fibrosis airway.Natural product reports · 2026Review
- Retrospective analysis of secreted PrpL protease activity in clinical isolates ofFrontiers in microbiology · 2026Article
- Comparative inhibitory effects of phillyrin and phillygenin on elastase: mechanisms and therapeutic potential.Frontiers in nutrition · 2026Article
- Microbial phenazines: biosynthesis, structural diversity, evolution, regulation, and biological significance.Microbiology and molecular biology reviews : MMBR · 2025Review
- Systems-level exploitation of OxyR regulon unravels a potential antibacterial target in Pseudomonas aeruginosa.Communications biology · 2025Article
- A phenazine-inspired framework for identifying biological functions of microbial redox-active metabolites.Current opinion in chemical biology · 2023Review
- A purified and lyophilized Pseudomonas aeruginosa derived pyocyanin induces promising apoptotic and necrotic activities against MCF-7 human breast adenocarcinoma.Microbial cell factories · 2022Article
- Quorum sensing inhibitory effect of bergamot oil and aspidosperma extract against Chromobacterium violaceum and Pseudomonas aeruginosa.Archives of microbiology · 2021Article
- Quorum sensing systems, related virulence factors, and biofilm formation in Pseudomonas aeruginosa isolated from fish.Archives of microbiology · 2021Article
- Phenazines as potential biomarkers of Pseudomonas aeruginosa infections: synthesis regulation, pathogenesis and analytical methods for their detection.Analytical and bioanalytical chemistry · 2020Review
- Article
- Signaling Natural Products from Human Pathogenic Bacteria.ACS infectious diseases · 2020Review
- Availability of Zinc Impacts Interactions between Streptococcus sanguinis and Pseudomonas aeruginosa in Coculture.Journal of bacteriology · 2020Article
- Electric Field Based Dressing Disrupts Mixed-Species Bacterial Biofilm Infection and Restores Functional Wound Healing.Annals of surgery · 2019Article
- Bacterial Biofilm Control by Perturbation of Bacterial Signaling Processes.International journal of molecular sciences · 2017Review
- Review
- Virulence Factors of Pseudomonas aeruginosa Induce Both the Unfolded Protein and Integrated Stress Responses in Airway Epithelial Cells.PLoS pathogens · 2015Article
- Functional amyloids keep quorum-sensing molecules in check.The Journal of biological chemistry · 2015Article
- Article
- Pyocyanin-induced mucin production is associated with redox modification of FOXA2.Respiratory research · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Alpha1 Protease inhibitor (alpha1PI) modulates serine protease activity in the lung. Reactive oxygen species inactivate alpha1PI, and this process has been implicated in the pathogenesis of a variety of forms of lung injury. An imbalance of protease-antiprotease activity is also detected in the airways of patients with cystic fibrosis-associated lung disease who are infected with Pseudomonas aeruginosa. P. aeruginosa secretes pyocyanin, which, through its ability to redox cycle, induces cells to generate reactive oxygen species. We tested the hypothesis that redox cycling of pyocyanin could lead to inactivation of alpha1PI. When alpha1PI was exposed to NADH and pyocyanin, a combination that results in superoxide production, alpha1PI lost its ability to form an inhibitory complex with both porcine pancreatic elastase (PPE) and trypsin. Similarly, addition of pyocyanin to cultures of human airway epithelial cells to which alpha1PI was also added resulted in a loss of the ability of alpha1PI to form a complex with PPE or trypsin. Neither superoxide dismutase, catalase, nor dimethylthiourea nor depletion of the media of O2 to prevent formation of reactive oxygen species blocked pyocyanin-mediated inactivation of alpha1PI. These data raise the possibility that a direct interaction between reduced pyocyanin and alpha1PI is involved in the process. Consistent with this possibility, pretreatment of alpha1PI with the reducing agent beta-mercaptoethanol also inhibited binding of trypsin to alpha1PI. These data suggest that pyocyanin could contribute to lung injury in the P. aeruginosa-infected airway of cystic fibrosis patients by decreasing the ability of alpha1PI to control the local activity of serine proteases.
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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.