title: Increased expression of C-reactive protein gene in inflamed gingival tissues could be derived from endothelial cells stimulated with interleukin-6.
abstract: BACKGROUND
  Epidemiological studies have suggested periodontitis as a risk factor for ischemic heart disease. High sensitive C-reactive protein (hs-CRP), a predictor of cardiovascular risk, is elevated in periodontitis patients. Therefore, local infection-induced elevation of systemic CRP could account for the relationship between the 2 diseases. However, the underlying mechanism of CRP production in the periodontal tissues has not been fully elucidated. Therefore, the aim of the present study was to clarify the mechanism of CRP production in periodontal tissues.
  
  
  METHODS
  Gene expression of CRP in gingival biopsies was analysed by quantitative PCR. Human gingival epithelial cells (HGECs), human gingival fibroblasts (HGFBs), and human coronary artery endothelial cells (HCAECs) were characterized for CRP-producing ability by incubating with interleukin (IL)-1β, IL-6, soluble IL-6 receptor (sIL-6R), and Porphyromonas gingivalis strain W83.
  
  
  RESULTS
  Gene expression of CRP is significantly elevated in periodontitis lesions compared with gingivitis lesions. HCAECs, but not HGECs and HGFBs, produced CRP in response to IL-6 and IL-1β in the presence of sIL-6R. In contrast to IL-6, the effect of IL-1β on CRP production was indirect via induction of IL-6. IL-1β was produced by HGECs and HGFBs with stimulation of P. gingivalis antigens.
  
  
  CONCLUSIONS
  These results suggest that CRP induced locally by periodontal infection may play another role in the pathogenesis of periodontal disease, and to a much lesser extent, has the potential to modulate systemic CRP level by extra-hepatic CRP production.
authors.affiliation: Center for Transdisciplinary Research, Niigata University, 2-5274 Gakko-cho, Chuo -ku, Niigata 951-8514, Japan.
authors.forename: Tomoki
authors.initials: T
authors.lastname: Maekawa
authors.forename: Koichi
authors.initials: K
authors.lastname: Tabeta
authors.forename: Keiko
authors.initials: K
authors.lastname: Kajita-Okui
authors.forename: Takako
authors.initials: T
authors.lastname: Nakajima
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Yamazaki
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D002097:C-Reactive Protein / Q000096:biosynthesis* / Q000235:genetics; D016022:Case-Control Studies; D002478:Cells, Cultured; D055113:Chronic Periodontitis / Q000378:metabolism; D003331:Coronary Vessels / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D042783:Endothelial Cells / Q000187:drug effects* / Q000378:metabolism; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism; D015870:Gene Expression; D005881:Gingiva / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D005891:Gingivitis / Q000378:metabolism; D006801:Humans; D053583:Interleukin-1beta / Q000494:pharmacology; D015850:Interleukin-6 / Q000096:biosynthesis / Q000494:pharmacology*; D008875:Middle Aged; D010512:Periodontal Index; D016966:Porphyromonas gingivalis; D019947:Receptors, Interleukin-6 / Q000502:physiology*
chemical_list: C508603:IL6R protein, human; D053583:Interleukin-1beta; D015850:Interleukin-6; D019947:Receptors, Interleukin-6; D002097:C-Reactive Protein