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Updated: May 31, 2026
Isolation, Characterization and Functional Examination of the Gingival Immune Cell Network
Published on: February 16, 2016
Quest for anti-inflammatory substances using IL-1β-stimulated gingival fibroblasts
Manami Ono1, Kaori Kantoh, Junichi Ueki
1Faculty of Science, Josai University, Sakado, Saitama 350-0295, Japan.
Background:
We have previously reported that azulene-related compounds, and alkaline extract of Sasa senanensis Rehder potently inhibited nitric oxide (NO) production by lipopolysaccharide (LPS)-stimulated mouse macrophages. We investigated here whether they can inhibit pro-inflammatory cytokine production, by activated human gingival fibroblast (HGF).
Materials And Methods:
HGF was established from the periodontal tissues of extracted tooth. Viable cell number was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method. Production of Prostaglandin E(2) (PGE(2)) and cytokines was determined by enzyme immunoassay, and enzyme-linked immunosorbent assay, respectively.
Results:
Interleukin (IL)-1β did not inhibit, but rather slightly stimulated the growth of HGF cells. IL-1β stimulated the production of PGE(2), IL-6, IL-8 and monocyte chemotactic protein-1 very potently, but not that of nitric oxide and tumor necrosis factor-α. Native LPS and synthetic lipid A from E. coli and P. gingivalis was much less stimulatory. Dexamethasone, not indomethacin, was an efficient inhibitor of IL-8 production. Among five azulene-related compounds, benzo[b]cyclohepta[e][1,4]thiazine most potently inhibited the IL-8 production by HGF cells, as well as NO production by activated RAW264.7 cells. The alkaline extract of Sasa senanensis Rehder significantly inhibited IL-8 production, without affecting the cell viability.
Conclusion:
The present system may be applicable for use in the search for anti-gingivitis substances.
