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Tobacco‐induced alterations to Porphyromonas gingivalis –host interactions
Author(s) -
Bagaitkar Juhi,
Williams Lisa R.,
Renaud Diane E.,
Bemakanakere Manjunatha R.,
Martin Mike,
Scott David A.,
Demuth Donald R.
Publication year - 2009
Publication title -
environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.954
H-Index - 188
eISSN - 1462-2920
pISSN - 1462-2912
DOI - 10.1111/j.1462-2920.2008.01852.x
Subject(s) - porphyromonas gingivalis , biology , virulence , microbiology and biotechnology , proinflammatory cytokine , virulence factor , bacterial outer membrane , gene , pathogen , tumor necrosis factor alpha , periodontitis , immunology , inflammation , bacteria , genetics , medicine , escherichia coli
Summary Smokers are more susceptible than non‐smokers to persistent infection by Porphyromonas gingivalis , a causative agent of periodontitis. Patients who smoke exhibit increased susceptibility to periodontitis and are more likely to display severe disease and be refractory to treatment. Paradoxically, smokers demonstrate reduced clinical inflammation. We show that P. gingivalis cells exposed to cigarette smoke extract (CSE) induce a lower proinflammatory response (tumour necrosis factor‐α, interleukin‐6, interleukin‐12 p40) from monocytes and peripheral blood mononuclear cells than do unexposed bacteria. This effect is reversed when CSE‐exposed bacteria are subcultured in fresh medium without CSE. Using microarrays representative of the P. gingivalis genome, CSE‐exposure resulted in differential regulation of 6.8% of P. gingivalis genes, including detoxification and oxidative stress‐related genes; DNA repair genes; and multiple genes related to P. gingivalis virulence, including genes in the major fimbrial and capsular operons. Exposure to CSE also altered the expression of outer membrane proteins, most notably by inducing the virulence factors RagA and RagB, and a putative lipoprotein cotranscribed with the minor fimbrial antigen. Therefore, CSE represents an environmental stress to which P. gingivalis adapts by altering gene expression and outer membrane proteins. These changes may explain, in part, the altered virulence and host–pathogen interactions that have been documented in vivo in smokers with periodontal disease.