Phenazines are small redox-active molecules produced by a variety of bacteria.  Beyond merely serving as antibiotics, they are increasingly recognized as having other, important physiological functions for the cells that produce them.  For example, by shuttling electrons from cellular reductants to poised-potential electrodes, endogenous phenazine �antibiotics� are key to anaerobic survival of the opportunistic pathogen Pseudomonas aeruginosa under oxidant-limited conditions (Wang Y., Kern S. E., and Newman D. K., J. Bacteriol. 192: 365, 2010).  Here we examine whether this relationship holds true with the naturally abundant Fe(III) hydroxide mineral (ferrihydrite) as the sole extracellular oxidant.  We show that phenazine-1-carboxylic acid can function as an electron shuttle to support anaerobic survival of P. aeruginosa via promoting ferrihydrite reduction, and thus render cells more resistant to antimicrobial drugs.  On the contrary, the phenazines pyocyanin and 1-hydroxyphenazine can drastically enhance anaerobic killing of P. aeruginosa via redox reactions with ferrihydrite that lead to Fe(II) production and phenazine degradation.  In addition, the killing efficiencies correlate with rates of Fe(III) reduction and phenazine degradation in response to different ferrihydrite and pheanazine concentrations.  Moreover, the induced killings render cells more susceptible to antimicrobial drugs in a synergistic manner.  Our results indicate that phenazine facilitated microbial Fe(III) reduction is a double-edged sword: while it can promote anaerobic survival, it can also exact a toxic price, depending on the nature of different phenazines and extracellular oxidants.

Phenazines differentially affect anaerobic survival and antimicrobial resistance of <i>Pseudomonas</i> bacteria via promoting Fe(III) reduction

243rd National Meeting (2012)

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Phenazines differentially affect anaerobic survival and antimicrobial resistance of Pseudomonas bacteria via promoting Fe(III) reduction