BACKGROUND AND OBJECTIVE: Porphyromonas gingivalis infection is strongly associated with periodontitis. Although P. gingivalis is known to elicit a strong inflammatory response, details of that remain fragmentary. To understand the local response to P. gingivalis, primary cell lines derived from mouse gingival tissues were exposed to P. gingivalis or Escherichia coli lipopolysaccharide, and the production of interleukin-6 and tumor necrosis factor-alpha was measured. CCL25 gene expression was measured by real-time polymerase chain reaction. Cells stimulated with combinations of interleukin-6, soluble interleukin-6 receptor and/or soluble gp130 were assayed for CCL2 and tumor necrosis factor-alpha secretion. MATERIAL AND METHODS: Primary cell lines were generated from mouse gingival tissues. Enzyme-linked immunosorbent assays were used to determine cytokine levels, and real-time polymerase chain reaction was used to quantify CCL25 gene expression. RESULTS: Exposure to P. gingivalis lipopolysaccharide but not to E. coli lipopolysaccharide resulted in significantly elevated levels of both interleukin-6 and tumor necrosis factor-alpha, and stimulation with P. gingivalis lipopolysaccharide also upregulated CCL25 gene expression. In one of three experiments, interleukin-6 induced CCL2 secretion, whereas interleukin-6 plus soluble interleukin-6 receptor induced CCL2 secretion in all three experiments, suggesting that both direct interleukin-6 signaling and interleukin-6 trans-signaling may be involved. However, because soluble gp130 did not inhibit trans-signaling, and because direct stimulation of gingival cells with soluble gp130 resulted in CCL2 secretion, the possibility exists that soluble gp130 forms binary complexes with soluble interleukin-6 receptor that promote direct interleukin-6 stimulation. CONCLUSION: These findings define a pathway in which exposure of gingival cells to P. gingivalis induces the release of interleukin-6 and tumor necrosis factor-alpha; interleukin-6, in turn, induces CCL2 secretion.
BACKGROUND AND OBJECTIVE:Porphyromonas gingivalis infection is strongly associated with periodontitis. Although P. gingivalis is known to elicit a strong inflammatory response, details of that remain fragmentary. To understand the local response to P. gingivalis, primary cell lines derived from mouse gingival tissues were exposed to P. gingivalis or Escherichia colilipopolysaccharide, and the production of interleukin-6 and tumor necrosis factor-alpha was measured. CCL25 gene expression was measured by real-time polymerase chain reaction. Cells stimulated with combinations of interleukin-6, soluble interleukin-6 receptor and/or soluble gp130 were assayed for CCL2 and tumor necrosis factor-alpha secretion. MATERIAL AND METHODS: Primary cell lines were generated from mouse gingival tissues. Enzyme-linked immunosorbent assays were used to determine cytokine levels, and real-time polymerase chain reaction was used to quantify CCL25 gene expression. RESULTS: Exposure to P. gingivalislipopolysaccharide but not to E. colilipopolysaccharide resulted in significantly elevated levels of both interleukin-6 and tumor necrosis factor-alpha, and stimulation with P. gingivalislipopolysaccharide also upregulated CCL25 gene expression. In one of three experiments, interleukin-6 induced CCL2 secretion, whereas interleukin-6 plus soluble interleukin-6 receptor induced CCL2 secretion in all three experiments, suggesting that both direct interleukin-6 signaling and interleukin-6 trans-signaling may be involved. However, because soluble gp130 did not inhibit trans-signaling, and because direct stimulation of gingival cells with soluble gp130 resulted in CCL2 secretion, the possibility exists that soluble gp130 forms binary complexes with soluble interleukin-6 receptor that promote direct interleukin-6 stimulation. CONCLUSION: These findings define a pathway in which exposure of gingival cells to P. gingivalis induces the release of interleukin-6 and tumor necrosis factor-alpha; interleukin-6, in turn, induces CCL2 secretion.
Authors: P L Wang; M Oido-Mori; T Fujii; Y Kowashi; M Kikuchi; Y Suetsugu; J Tanaka; Y Azuma; M Shinohara; K Ohura Journal: Biochem Biophys Res Commun Date: 2001-11-09 Impact factor: 3.575
Authors: S M Hurst; T S Wilkinson; R M McLoughlin; S Jones; S Horiuchi; N Yamamoto; S Rose-John; G M Fuller; N Topley; S A Jones Journal: Immunity Date: 2001-06 Impact factor: 31.745
Authors: B A Zabel; W W Agace; J J Campbell; H M Heath; D Parent; A I Roberts; E C Ebert; N Kassam; S Qin; M Zovko; G J LaRosa; L L Yang; D Soler; E C Butcher; P D Ponath; C M Parker; D P Andrew Journal: J Exp Med Date: 1999-11-01 Impact factor: 14.307
Authors: E J Kunkel; J J Campbell; G Haraldsen; J Pan; J Boisvert; A I Roberts; E C Ebert; M A Vierra; S B Goodman; M C Genovese; A J Wardlaw; H B Greenberg; C M Parker; E C Butcher; D P Andrew; W W Agace Journal: J Exp Med Date: 2000-09-04 Impact factor: 14.307
Authors: Katy J Jones; Sanaz Ekhlassi; Dina Montufar-Solis; John R Klein; Jeremy S Schaefer Journal: J Periodontol Date: 2010-09-15 Impact factor: 6.993