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.

Staphylococcus aureus responds with protective strategies against phagocyte-derived reactive oxidants to infect humans. Herein, we report the transcriptome analysis of the cellular response of S. aureus to hydrogen peroxide-induced oxidative stress. The data indicate that the oxidative response includes the induction of genes involved in virulence, DNA repair, and notably, anaerobic metabolism.

Sodium hypochlorite (bleach) is routinely used in hospitals and health care facilities for surface sterilization; however, the mechanism of action by which this disinfectant kills and the extent to which Pseudomonas aeruginosa is resistant to sodium hypochlorite have not been elucidated. Consequently, nosocomial infections from P. aeruginosa result in considerable casualties and economic hardship. We report the genome-wide transcriptome response of P. aeruginosa to sodium hypochlorite-induced oxidative stress via the use of DNA microarrays. In addition to a general oxidative stress response, our data revealed a downregulation of virtually all genes related to oxidative phosphorylation and electron transport and an upregulation of many organic sulfur transport and metabolism genes.

Disinfectants are routinely used in hospitals and health care facilities for surface sterilization. However, the mechanisms by which these disinfectants kill and the extent to which bacteria, including Pseudomonas aeruginosa, are resistant remains unclear. Consequently, P. aeruginosa nosocomial infections result in considerable casualties and economic hardship. Previously, DNA microarrays were utilized to analyze the genome-wide transcription changes in P. aeruginosa after oxidative antimicrobial (sodium hypochlorite, peracetic acid, and hydrogen peroxide) exposure. Simultaneous analysis of these transcriptome datasets provided a comprehensive understanding of the differential responses to these disinfectants. An analysis of variance, functional classification analysis, metabolic pathway analysis, Venn diagram analysis, and principal component analysis revealed that sodium hypochlorite exposure resulted in more genome-wide changes than either peracetic acid or hydrogen peroxide exposures.

Pseudomonas aeruginosa is implicated in nosocomial infections and chronic respiratory infections in cystic fibrosis patients. Chlorhexidine diacetate (CHX) is a biguanide disinfectant used for bacterial control in the hospital and agricultural and domestic environments. A better understanding of the mechanism of action of CHX and the resulting response elicited by P. aeruginosa to CHX will facilitate its effective utilization for P. aeruginosa control in these environments. This study presents, for the first time, the transcriptomic response of P. aeruginosa to 0.008 mM CHX after 10 and 60 min. Our results reveal that, after both treatment times, membrane transport, oxidative phosphorylation, and electron transport genes were downregulated. After 10 min, DNA repair was downregulated and the oprH gene that blocks the self-promoted uptake of antimicrobials was upregulated. After 60 min, outer membrane protein, flagellum, pilus, oxidative phosphorylation, and electron transport genes were downregulated. The mexC and mexD genes of the MexCD-OprJ multidrug efflux pump were significantly upregulated after both treatment times. The results of this study improve our understanding of the mode of action of CHX on P. aeruginosa and provide insights into the mechanism of action of other biguanide disinfectants which can be used for the development of more efficient disinfectants.