Tobacco‐induced alterations to Porphyromonas gingivalis–host interactions

Abstract

SUMMARYSmokers 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 pro-inflammatory response (TNF-α, IL-6, IL12 p40) from monocytes and PBMCs 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 co-transcribed 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.

Advanced Glycation End Products: Possible Link Between Metabolic Syndrome and Periodontal Diseases

“…Contemporary literature supports the assumption that, in addition to inflammation and oxidative stress, other conditions such as cigarette smoking (Bagaitkar et al, 2009), vitamin deficits, alcohol abuse, diet (Dye, 2010;Hujoel, 2009), and other pro-oxidation conditions, such as MetS, play a key role in the activation of signalling pathways, which act in promoting ROS development and probably also in worsening or producing new onset of a periodontal disease (Liu et al, 2011;Soory, 2009;Boden, 2006).…”

Porphyromonas gingivalis infection in gestational diabetes mellitus and survival in tobacco smokers.

“…Because of down-regulation of antiinflammatory factors along with an upregulation of pro-inflammatory cytokines, there might be increased infection risk by periodontal pathogens in smokers. Smokers are susceptible to colonization by P. gingivalis, a causative agent of periodontitis [180].…”

“…gingivalis adapts to the environmental stress induced by CSE by altering the expression of several genes and outer membrane proteins [180]. To withstand these adverse effects, there might be upregulation of certain genes for the repair of damaged organelles.…”

“…Bagaitkar et al, it has been shown that CSE significantly influences the expression of 6.8% of the P. gingivalis genome, as determined by whole genome arrays [180]. These included genes regulating capsule and fimbriae, corresponding to the reduced proinflammatory potential of P. gingivalis; oxidative stress and DNA repair.…”

“…These included genes regulating capsule and fimbriae, corresponding to the reduced proinflammatory potential of P. gingivalis; oxidative stress and DNA repair. P. gingivalis adapts to the environmental stress presented by CSE by altering the expression of several genes and outer membrane proteins [180].…”