PMID- 10948156
OWN - NLM
STAT- MEDLINE
DCOM- 20000908
LR  - 20210526
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 68
IP  - 9
DP  - 2000 Sep
TI  - Cytokine responses to treponema pectinovorum and treponema denticola in human 
      gingival fibroblasts.
PG  - 5284-92
AB  - Human gingival fibroblasts were challenged with Treponema pectinovorum and 
      Treponema denticola to test three specific hypotheses: (i) these treponemes 
      induce different cytokine profiles from the fibroblasts, (ii) differences in 
      cytokine profiles are observed after challenge with live versus killed 
      treponemes, and (iii) differences in cytokine profiles are noted from different 
      gingival fibroblast cell lines when challenged with these treponemes. Three 
      normal gingival fibroblast cell cultures were challenged with T. pectinovorum and 
      T. denticola strains, and the supernatants were analyzed for cytokine production 
      (i.e., interleukin-1alpha [IL-1alpha], IL-1beta, IL-6, IL-8, IL-10, gamma 
      interferon, macrophage chemotactic protein 1 [MCP-1], platelet-derived growth 
      factor, tumor necrosis factor alpha, and granulocyte-macrophage 
      colony-stimulating factor). Unstimulated fibroblast cell lines produced IL-6, 
      IL-8, and MCP-1. T. pectinovorum routinely elicited the greatest production of 
      these cytokines from the fibroblast cell lines, increasing 10- to 50-fold over 
      basal production. While T. denticola also induced IL-6 and IL-8 production, these 
      levels were generally lower than those elicited by challenge with T. 
      pectinovorum. MCP-1 levels were significantly lower after T. denticola challenge, 
      and the kinetics suggested that this microorganism actually inhibited basal 
      production by the fibroblasts. No basal or stimulated production of the other 
      cytokines was observed. Significant differences were noted in the responsiveness 
      of the various cell lines with respect to the two species of treponemes and the 
      individual cytokines produced. Finally, dead T. pectinovorum generally induced a 
      twofold-greater level of IL-6 and IL-8 than the live bacteria. These results 
      supported the idea that different species of oral treponemes can elicit 
      proinflammatory cytokine production by gingival cells and that this stimulation 
      did not require live microorganisms. Importantly, a unique difference was noted 
      in the ability of T. pectinovorum to induce a robust MCP-1 production, while T. 
      denticola appeared to inhibit this activity of the fibroblasts. While the general 
      cytokine profiles of the fibroblast cell cultures were similar, significant 
      differences were noted in the quantity of individual cytokines produced, which 
      could relate to individual patient variation in local inflammatory responses in 
      the periodontium.
FAU - Nixon, C S
AU  - Nixon CS
AD  - Departments of Microbiology, University of Texas Health Science Center at San 
      Antonio, San Antonio, Texas 78284, USA.
FAU - Steffen, M J
AU  - Steffen MJ
FAU - Ebersole, J L
AU  - Ebersole JL
LA  - eng
GR  - R01 DE011368/DE/NIDCR NIH HHS/United States
GR  - DE11368/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukin-8)
SB  - IM
MH  - Chemokine CCL2/biosynthesis
MH  - Cytokines/*biosynthesis
MH  - Fibroblasts/immunology/microbiology
MH  - Gingiva/*immunology/*microbiology
MH  - Humans
MH  - Interleukin-6/biosynthesis
MH  - Interleukin-8/biosynthesis
MH  - Treponema/*physiology
PMC - PMC101790
EDAT- 2000/08/19 11:00
MHDA- 2000/09/19 11:01
PMCR- 2000/09/01
CRDT- 2000/08/19 11:00
PHST- 2000/08/19 11:00 [pubmed]
PHST- 2000/09/19 11:01 [medline]
PHST- 2000/08/19 11:00 [entrez]
PHST- 2000/09/01 00:00 [pmc-release]
AID - 1681 [pii]
AID - 10.1128/IAI.68.9.5284-5292.2000 [doi]
PST - ppublish
SO  - Infect Immun. 2000 Sep;68(9):5284-92. doi: 10.1128/IAI.68.9.5284-5292.2000.