UC San Diego

In the United States, cigarette smoking holds a significant portion of preventable causes of death and disease. Studies have shown that cigarette smoke can modify the human defense system as well as leading the cigarette smoker to have higher risk bacterial infection. However, the field of host-pathogen interactions after exposure to cigarette smoke is still poorly understood. In this study, we focus on the effects of cigarette smoke on the virulent properties of Pseudomonas aeruginosa (PSA), an important airway pathogen that is extremely detrimental to cystic fibrosis and immunocompromised patients. We uncover that PSA exposed to cigarette smoke extract (CSE) demonstrated increase antibiotic resistance to levofloxacin and gentamicin. In our current paper under review, we have demonstrated that PSA exposed to CSE (CSE-PSA) showed increase resistance to oxidative burst by neutrophil and hydrogen peroxide treatment. To examine the underlying mechanism of these increases in virulence, RT-qPCR was used on control- and CSE-PSA to observe changes in gene expression. Genes that encode parts and regulation of PSA efflux pumps (mexA, mexX, mexZ) showed increased gene expression in CSE-PSA over control-PSA. Of three oxidative stress response genes (gpx, oxyR, tpx), only tpx, a gene encoding a thiol peroxidase homolog, demonstrated statistical significance. However, all three genes showed a trend of overall increase, suggesting that cigarette smoke is inducing changes in PSA gene expression. We conclude that cigarette smoke increases virulence in PSA virulence by increasing gene expression involved in antibiotic resistance and oxidative stress.