Date on Master's Thesis/Doctoral Dissertation


Document Type

Doctoral Dissertation

Degree Name

Ph. D.


Microbiology and Immunology

Committee Chair

Scott, David Albert

Author's Keywords

Tobacco; Porphyromonas gingivalis; Biofilms; Host-pathogen interactions; Smoke; Periodontitis; Inflammation


Porphyromonas gingivalis; Periodontium--Infections; Tobacco--Physiological effect; Tobacco use--Physiological aspects


Tobacco smoke is a strong and independent risk factor for several chronic systemic diseases and also increases susceptibility to a multitude of bacterial infections, including periodontal infections. Periodontitis is a chronic inflammatory disease of the supporting tissues of the periodontium caused by its chief etiological agent, Porphyromonas gingivalis . Smokers are more prone to persistent infections by P. gingivalis , and harbor higher numbers of P. gingivalis than non-smokers. However, smokers show reduced clinical signs of inflammation compared to non-smokers, making diagnosis of periodontal disease in smokers problematic. While several studies delineate the different mechanisms of how tobacco smoke alters host response to periodontitis, very little is known about its effects on the virulence profile of P. gingivalis . We hypothesize, that tobacco smoke presents an environmental stress to which P. gingivalis adapts by altering its gene expression, which in turn will influence its interaction with the host. Indeed, P. gingivalis microarray and qRT-PCR data show that about 7% of P. gingivalis genes are differentially regulated on exposure to cigarette smoke extract (CSE) including major and minor fimbrial antigens (FimA and Mfa1, respectively) and capsule. CSE- induced phenotypic alterations are consistent with increased biofim formation and reduced pro-inflammatory potential of intact P. gingivalis . Furthermore chronic exposure to P. gingivalis FimA leads to the abrogation of the pro-inflammatory response in a TLR2- and IRAK1 dependent manner. These studies provide some of the first information to explain, mechanistically, how tobacco smoke changes the P. gingivalis phenotype in a manner likely to promote P. gingivalis colonization and infection while simultaneously reducing the host response to this major mucosal pathogen.