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Alterations in Pathogenicity Factors of Pseudomonas aeruginosa in Response to Cigarette Smoke Exposure


Cigarette smoking is one of the leading preventable causes of death in the United States. It is well recognized that cigarette smoking alters the human defense mechanism, and increases susceptibility to bacterial infections and diseases, such as pneumonia and chronic obstructive pulmonary disease. However, the effects of cigarette smoke on the pathogenic aspect of this human-pathogen dynamic remains poorly understood. Therefore, we sought to determine the effects of cigarette smoke on the pathogenicity properties of Pseudomonas aeruginosa (PSA), a prominent airway pathogen in adult smokers. Here, we show that while cigarette smoke exposure slows PSA growth in a dose-dependent manner, it increases certain pathogenicity factors. PSA exposed to cigarette smoke extract (CSE) showed increased resistance to killing by reactive oxygen species, suggesting that cigarette smoke may aid in the survival of PSA in phagolysosomes, a principal innate immune antimicrobial mechanism. When human neutrophils were infected with PSA, cigarette smoke exposure increased resistance to neutrophil killing, with 100% of CSE-PSA surviving, while 20% of control PSA was killed. Furthermore, we discovered that a long-term CSE exposure causes a more dramatic inhibition in PSA growth, compared to PSA with one time CSE exposure; this suggests that the PSA population in long-term smokers may possess different virulence properties than their sporadic/non-smoker counterparts. We conclude that cigarette smoke-induced resistance phenotypes in pathogens may be an important contributor to the vulnerability of cigarette smokers to infectious airway diseases. We hope our findings will improve our understanding of the effects of cigarette smoke on human health.

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