Research article
Microarray analysis of Pseudomonas aeruginosa reveals induction of pyocin genes in response to hydrogen peroxide
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* Corresponding author: Freshteh Toghrol toghrol.freshteh@epa.gov
1 Center for Biosystems Research, University of Maryland Biotechnology Institute, College Park, Maryland 20742, USA
2 Microarray Research Laboratory, Biological and Economic Analysis Division, Office of Pesticide Programs, U. S. Environmental Protection Agency, Fort Meade, Maryland 20755, USA
BMC Genomics 2005, 6:115 doi:10.1186/1471-2164-6-115
Published: 8 September 2005Abstract
Background
Pseudomonas aeruginosa, a pathogen infecting those with cystic fibrosis, encounters toxicity from phagocyte-derived reactive oxidants including hydrogen peroxide during active infection. P. aeruginosa responds with adaptive and protective strategies against these toxic species to effectively infect humans. Despite advances in our understanding of the responses to oxidative stress in many specific cases, the connectivity between targeted protective genes and the rest of cell metabolism remains obscure.
Results
Herein, we performed a genome-wide transcriptome analysis of the cellular responses to hydrogen peroxide in order to determine a more complete picture of how oxidative stress-induced genes are related and regulated.
Our data reinforce the previous conclusion that DNA repair proteins and catalases may be among the most vital antioxidant defense systems of P. aeruginosa. Our results also suggest that sublethal oxidative damage reduces active and/or facilitated transport and that intracellular iron might be a key factor for a relationship between oxidative stress and iron regulation. Perhaps most intriguingly, we revealed that the transcription of all F-, R-, and S-type pyocins was upregulated by oxidative stress and at the same time, a cell immunity protein (pyocin S2 immunity protein) was downregulated, possibly leading to self-killing activity.
Conclusion
This finding proposes that pyocin production might be another novel defensive scheme against oxidative attack by host cells.