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Updated: Aug 23, 2026

Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice
Published on: March 17, 2014
Pseudomonas aeruginosa pyocyanin is critical for lung infection in mice
Gee W Lau1, Huimin Ran, Fansheng Kong
1Division of Pulmonary and Critical Care Medicine, University of Cincinnati College of Medicine, 231 Albert Sabin Way, MSB 6006, Cincinnati, OH 45267-0564, USA. gee.lau@uc.edu
Abstract:
Pseudomonas aeruginosa secretes copious amounts of the redox-active phenazine, pyocyanin (PCN), during cystic fibrosis lung infection. PCN has been shown to interfere with a variety of cellular processes in cultured lung epithelial cells. Here, by using two respiratory tract models of infection, we demonstrate that PCN mediates tissue damage and necrosis during lung infection.
Insights
Pseudomonas aeruginosa releases pyocyanin (PCN) during lung infections. This study shows PCN causes tissue damage and cell death in respiratory tract models.
Area of Science:
- Microbiology
- Pathogenesis
- Respiratory Medicine
Background:
- Pseudomonas aeruginosa is a common opportunistic pathogen, particularly in cystic fibrosis lung infections.
- The bacterium produces pyocyanin (PCN), a redox-active phenazine compound.
- PCN is known to affect cellular functions in lung epithelial cells in vitro.
Purpose of the Study:
- To investigate the role of pyocyanin (PCN) in mediating tissue damage during respiratory tract infections.
- To validate the pathogenic effects of PCN in relevant in vivo models.
Main Methods:
- Utilized two distinct respiratory tract models of infection.
- Assessed tissue damage and necrosis in the presence of PCN.
Main Results:
- Demonstrated that pyocyanin (PCN) directly mediates tissue damage.
- Confirmed PCN's role in inducing necrosis within the respiratory tract models.
Conclusions:
- Pyocyanin (PCN) is a key virulence factor contributing to lung tissue damage and necrosis during Pseudomonas aeruginosa infections.
- These findings highlight PCN as a potential therapeutic target for mitigating infection-induced lung injury.

