title: Altered antigenic profiling and infectivity of Porphyromonas gingivalis in smokers and non-smokers with periodontitis.
abstract: BACKGROUND
  Cigarette smokers are more susceptible to periodontal diseases and are more likely to be infected with Porphyromonas gingivalis than non-smokers. Furthermore, smoking is known to alter the expression of P. gingivalis surface components and compromise immunoglobulin (Ig)G generation. The aim of this study is to evaluate whether the overall IgG response to P. gingivalis is suppressed in smokers in vivo and whether previously established in vitro tobacco-induced phenotypic P. gingivalis changes would be reflected in vivo.
  
  
  METHODS
  The authors examined the humoral response to several P. gingivalis strains as well as specific tobacco-regulated outer membrane proteins (FimA and RagB) by enzyme-linked immunosorbent assay in biochemically validated (salivary cotinine) smokers and non-smokers with chronic periodontitis (CP: n = 13) or aggressive periodontitis (AgP: n = 20). The local and systemic presence of P. gingivalis DNA was also monitored by polymerase chain reaction.
  
  
  RESULTS
  Smoking was associated with decreased total IgG responses against clinical (10512, 5607, and 10208C; all P <0.05) but not laboratory (ATCC 33277, W83) P. gingivalis strains. Smoking did not influence IgG produced against specific cell-surface proteins, although a non-significant pattern toward increased total FimA-specific IgG in patients with CP, but not AgP, was observed. Seropositive smokers were more likely to be infected orally and systemically with P. gingivalis (P <0.001), as determined by 16S RNA analysis.
  
  
  CONCLUSIONS
  Smoking alters the humoral response against P. gingivalis and may increase P. gingivalis infectivity, strengthening the evidence that mechanisms of periodontal disease progression in smokers may differ from those of non-smokers with the same disease classification.
authors.affiliation: Oral Health and Systemic Disease, University of Louisville, Louisville, KY.
authors.forename: Iris
authors.initials: I
authors.lastname: Zeller
authors.forename: Justin A
authors.initials: JA
authors.lastname: Hutcherson
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Lamont
authors.forename: Donald R
authors.initials: DR
authors.lastname: Demuth
authors.forename: Pinar
authors.initials: P
authors.lastname: Gumus
authors.forename: Nejat
authors.initials: N
authors.lastname: Nizam
authors.forename: Nurcan
authors.initials: N
authors.lastname: Buduneli
authors.forename: David A
authors.initials: DA
authors.lastname: Scott
mesh_terms: D000328:Adult; D010520:Aggressive Periodontitis / Q000276:immunology / Q000382:microbiology*; D000907:Antibodies, Bacterial / Q000276:immunology; D000942:Antigens, Bacterial / Q000276:immunology*; D001426:Bacterial Proteins / Q000276:immunology; D016866:Bacteroidaceae Infections / Q000276:immunology / Q000382:microbiology; D055113:Chronic Periodontitis / Q000276:immunology / Q000382:microbiology*; D003367:Cotinine / Q000032:analysis; D004269:DNA, Bacterial / Q000032:analysis; D003774:Dental Plaque Index; D005260:Female; D036781:Fimbriae Proteins / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D008297:Male; D008875:Middle Aged; D010512:Periodontal Index; D010641:Phenotype; D018933:Pili, Sex / Q000276:immunology; D016966:Porphyromonas gingivalis / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity; D012463:Saliva / Q000737:chemistry; D012907:Smoking / Q000276:immunology*; D014026:Nicotiana
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D004269:DNA, Bacterial; D007074:Immunoglobulin G; C545438:Mfa1 protein, Porphyromonas gingivalis; C484346:RagB protein, bacteria; C063055:fimbrillin; D036781:Fimbriae Proteins; D003367:Cotinine
keywords: Antigen-antibody reactions; Porphyromonas gingivalis; immunoglobulin; periodontitis; smoking; vaccines