title: The role of Desulfovibrio desulfuricans lipopolysaccharides in modulation of periodontal inflammation through stimulation of human gingival fibroblasts.
abstract: OBJECTIVE
  Periodontitis is a destructive disease which is likely to be the result of the activities of different microbial complexes. Recently, sulphate-reducing bacteria (SRB) have been detected in the oral cavity, and they have been found to be common inhabitants of sites showing periodontal destruction. The aim of study was to evaluate the influence of endotoxins of Desulfovibrio desulfuricans bacteria on human gingival fibroblast HGF-1 line.
  
  
  METHODS
  The immunological response of gingival fibroblasts was evaluated by determination of their IL-6 and IL-8 secretion upon treatment with D. desulfuricans intestinal and type strain LPS, sodium butyrate (NaB) and IL-1beta. The amounts of cytokines were estimated by ELISA immunoassay. The influence of LPS and NaB on fibroblast proliferation was determined using the CyQUANT Cell Proliferation Assay Kit.
  
  
  RESULTS
  No significant growth inhibition of cells exposed to LPS was observed, except for the culture growing in the presence of intestinal strain endotoxin at the highest concentration (100 microg/ml). The secretion of IL-6 and IL-8 by fibroblasts was increased by D. desulfuricans endotoxins. Cells stimulated with proinflammatory cytokine 1L-1beta showed very high levels of both cytokines secretion. The release of IL-6 and IL-8 by cells in response to LPS and 1L-1beta was modulated by butyric acid.
  
  
  CONCLUSIONS
  The observed response of gingival fibroblasts to stimulation by endotoxin suggests that D. desulfuricans can be involved in the pathogenesis of periodontitis. Moreover, butyrate present in the oral cavity seems to have immunoregulatory effect on cytokine production by gingival fibroblasts under physiological conditions and during microbe-induced inflammation.
authors.affiliation: Department of Biopharmacy, Medical University of Silesia, Sosnowiec, Poland.
authors.forename: Zofia
authors.initials: Z
authors.lastname: Dzierzewicz
authors.forename: Joanna
authors.initials: J
authors.lastname: Szczerba
authors.forename: Jolanta
authors.initials: J
authors.lastname: Lodowska
authors.forename: Daniel
authors.initials: D
authors.lastname: Wolny
authors.forename: Arkadiusz
authors.initials: A
authors.lastname: Gruchlik
authors.forename: Arkadiusz
authors.initials: A
authors.lastname: Orchel
authors.forename: Ludmiła
authors.initials: L
authors.lastname: Weglarz
mesh_terms: D002087:Butyrates / Q000008:administration & dosage / Q000494:pharmacology; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects; D045285:Desulfovibrio desulfuricans / Q000145:classification / Q000502:physiology*; D005347:Fibroblasts / Q000187:drug effects* / Q000276:immunology; D005881:Gingiva / Q000166:cytology / Q000187:drug effects* / Q000276:immunology; D006801:Humans; D018836:Inflammation Mediators / Q000494:pharmacology; D053583:Interleukin-1beta / Q000494:pharmacology; D015850:Interleukin-6 / Q000032:analysis / Q000378:metabolism; D016209:Interleukin-8 / Q000187:drug effects / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D010518:Periodontitis / Q000276:immunology / Q000473:pathology; D011506:Proteins / Q000032:analysis
chemical_list: D002087:Butyrates; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D015850:Interleukin-6; D016209:Interleukin-8; D008070:Lipopolysaccharides; D011506:Proteins