Pyocyanin

Pyocyanin, which can reach concentrations of 100 µM in cystic fibrosis patients infected with P. aeruginosa, activates the aryl hydrocarbon receptor with a K_i value of 5.4 µM.¹ This induces the expression of both detoxifying enzymes, resulting in pyocyanin degradation, and cytokines that facilitate the clearance of bacteria.¹ Pyocyanin has been shown to accelerate neutrophil apoptosis in vitro, resulting in resolution of acute inflammation, which is beneficial for bacterial survival. It also induces a 10-fold acceleration of neutrophil apoptosis in vivo.² Pyocyanin production results in reduced bacterial clearance from the lungs of immunocompromised patients. It has also been reported to induce apoptosis in human lung epithelial cells and to induce premature cellular senescence in mammalian cells.³ Pyocyanin undergoes nonenzymatic reduction by NADPH, which produces hydrogen peroxide and depletes intracellular glutathione levels, causing oxidative stress in susceptible cells.⁴

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1. Moura-Alves, P., Faé, K., Houthuys, E., et al. AhR sensing of bacterial pigments regulates antibacterial defence. Nature 512(7515), 387-392 (2014).

2. Allen, L., Dockrell, D.H., Pattery, T., et al. Pyocyanin production by Pseudomonas aeruginosa induces neutrophil apoptosis and impairs neutrophil-mediated host defenses in vivo. J. Immunol. 174, 3643-3649 (2005).

3. Muller, M. Premature cellular senescence induced by pyocyanin, a redox-active Pseudomonas aeruginosa toxin. Free Radic. Biol. Med. 41, 1670-1677 (2006).

4. Muller, M. Pyocyanin induces oxidative stress in human endothelial cells and modulates the glutathione redox cycle. Free Radic. Biol. Med. 33(11), 1527-1533 (2002).