Skip to search boxSkip to navigationSkip to main content

Interleukin-1β Regulation of Adhesion Molecules on Human Gingival and Periodontal Ligament Fibroblasts

  • Brandon H. Joe
    ,
  • James L. Borke(corresponding author)
    ,
  • Meral Keskintepe
    ,
  • Philip J. Hanes
    ,
  • Jason M. Mailhot
    ,
  • Baldev B. Singh
*Corresponding author for this work
Scholary Output:
Contribution to journal
Article
Peer-review

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

Background: Adhesion molecules have been implicated in the pathogenesis of rheumatoid arthritis and may also play a role in the pathogenesis of periodontal disease by promoting the recruitment and retention of leukocytes in gingival tissue. Methods: The aim of the present study was to evaluate the capacity of interleukin-1β (IL-1β) to regulate adhesion molecule expression on clinically healthy human gingival (HGF) and periodontal ligament (PDL) fibroblasts. The HGF (n = 6) and PDL (n = 3) fibroblasts were treated with 1.0 ng/ml of IL-1β for 24 hours and then incubated with primary intercellular adhesion molecule-1 (ICAM-1) and vascular cellular adhesion molecule-1 (VCAM-1) antibodies followed by FITC-conjugated secondary antibodies. The expression of ICAM-1 and VCAM-1 was measured by immunofluorescence flow cytometry. Results: The levels of ICAM-1 expression in IL-1β treated HGF and PDL fibroblasts were statistically significant (P ≤0.05) compared to normal untreated controls using log-transformed data and 3-way analysis of variance. Both cells expressed VCAM-1 after IL-1β treatment, but the levels were not statistically different from controls. Conclusions: This study demonstrated that IL-1β upregulated ICAM-1 expression in both HGF and PDL fibroblasts. Even though the level of VCAM-1 was not statistically different from both HGF and PDL fibroblasts treated with IL-1β compared to controls, both cells do express the VCAM-1 molecules. These results suggest that ICAM-1 and VCAM-1 might be involved in the pathogenesis of periodontal disease.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 865-870 (6 pages)

Journal (Volume, Issue Number)

Journal of periodontology (Volume 72, Issue 7)

Publication milestones

  • Published - 07/2001

Publication status

Published - 07/2001

ISSN

0022-3492

Publication IDs

  • Scopus: 0035403373
  • PubMed: 11495133

Publication metrics

Metrics

Fractional count
1
Fractional count
0.17
Fractional count
5
Fractional count
0.83
Fractional count
1
Fractional count
1
SciVal
citations
22
Scopus
citations
SciVal
FWCI
0.31
SciVal
Author count
6
SciVal
Paper percentile
72

PlumX, opens in new tab

Captures
18
Citation count
26

Funding Details

FunderFunding number
NIDCR
R03DE012812