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Attenuation of butyric acid-induced T cell apoptosis by human gingival fibroblast

Research Project

Project/Area Number 11671818
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Morphological basic dentistry
Research InstitutionNihon University

Principal Investigator

OCHIAI Tamoko  NIHON UNIVERSITY, SCHOOL OF DENTISTRY AT MATSUDO, Lecturer, 松戸歯学部, 講師 (20130594)

Co-Investigator(Kenkyū-buntansha) OCHIAI Kuniyasu  MEIKAI UNIVERSITY SCHOOL OF DENTISTRY, Professor, 歯学部, 教授 (50095444)
Project Period (FY) 1999 – 2000
Project Status Completed (Fiscal Year 2000)
Budget Amount *help
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2000: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1999: ¥1,600,000 (Direct Cost: ¥1,600,000)
KeywordsAPOPTOSIS / T CELLS / FIBR OBLAST / BUTYRIC ACID / INFLAMMATORY CYTOKINES / CD44 / CD47 / CD58 / 揮発性脂肪酸 / 歯肉
Research Abstract

(1) Although butyric acid exhibited a dose-dependent inhibition in F41-G and Ca 9-22 cells, their effect was not prominent compared to the data with T-, B- and monocytic cells. Furthermore, the results of DNA fragmentation assay indicated that butyric acid did not induced apoptosis in human gingival fibroblasts (Gin 1, F41G and H.pulp).
(2) When the culture supernatants of gingival fibroblasts were assayed for IL-1α, IL-1β, IL-6, IL-8, IL-11, TNF α and TGF β by use of ELISA kits, butyric acid significautly increased IL-6, IL-8 and IL-11 production. Maximum levels of these cytokines were noted by the addition of 5 mM butyric acid in Gin 1, F41-G and H.pulp cells. These levels were 1,500 to 1,900 pg/ml (IL-6), ca.4,000 to 5,000 pg/ml (IL-8), and ca.900 to 1,100 pg/ml (IL-11).
(3) Co-culturing Jurkat cells with F41G or Gin 1 cells using intercup partially rescued butyric acid- or Fas-induced Jurkat cell apoptosis, suggest a role for a soluble factor released from fibroblasts in preventing T cell-apoptosis.
(4) IL-6 and IL-8 slightly stimulated butyric acid- or Fas-induced Jurkat cell apoptosis in a dose-dependent manner, in contrast, IL-11 significantly suppressed these Jurkat cell apoptosis dose-dependently. These results suggest that the sum of their effects of the inflammatory cytokines such as IL-6, IL-8 and IL-11, produced in fibroblast by the addition of butyric acid, are concernted in the attenuation of T cell apoptosis by gingival fibroblast.
(5) Furthemore, the direct cell-cell interaction indicated that the apoptosis of Jurkat T cells attached on the gingival fibroblasts was significantly rescued. CD47, CD44 and CD58 expression on the fibroblasts was increased by the addition of butyric acid, suggest that the increase of these cell surface molecule was concerned with the suppression of T cell apoptosis induced by butyric acid.

Report

(3 results)
  • 2000 Annual Research Report   Final Research Report Summary
  • 1999 Annual Research Report
  • Research Products

    (3 results)

All Other

All Publications (3 results)

  • [Publications] Tomoko Kurita-Ochiai: "Butyric-acid-induced apoptosis in murine thymocytes and splenic T- and B-cells occurs in the absence of p53."Journal of Dental Research. Vol,79. 1948-1954 (2000)

    • Related Report
      2000 Annual Research Report
  • [Publications] Tomoko Kurita-Ochiai: "Butyric acid-induced T cell apoptosis is mediated by caspase-8 and -9 activation in a Fas-independent manner"Clinical and Diagnostic Laboratory Immunology. Vol.8. In press (2001)

    • Related Report
      2000 Annual Research Report
  • [Publications] 栗田(落合)智子: "歯周病原性細菌とアポトーシス"化学療法の領域. 17巻. 148-157 (2001)

    • Related Report
      2000 Annual Research Report

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Published: 1999-04-01   Modified: 2016-04-21  

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