Infection and Immunity, December 1999, p. 6225-6233, Vol. 67, No. 12
Department of Endodontics and
Periodontics1 and Department of
Microbiology and Immunology,2 Tohoku
University School of Dentistry, Sendai, 980-8575, Japan
Received 11 March 1999/Returned for modification 18 May
1999/Accepted 1 September 1999
CD26/dipeptidyl peptidase IV (DPPIV) is a cell surface ectoenzyme
which participates in immune and inflammatory reactions. We found that
CD26 was only partially expressed on human fibroblasts from periodontal
tissues, whereas fibroblasts from lung and skin expressed CD26
constitutively as revealed by flow cytometry. We examined the possible
upregulation of CD26 expression on human gingival fibroblasts in
response to various stimulants. Interleukin-1
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Copyright © 1999, American Society for Microbiology. All rights reserved.
Increase of CD26/Dipeptidyl Peptidase IV Expression
on Human Gingival Fibroblasts upon Stimulation with Cytokines and
Bacterial Components
(IL-1
); tumor
necrosis factor alpha; gamma interferon; lipopolysaccharide from
Porphyromonas gingivalis, Prevotella
intermedia, and Escherichia coli; and
Prevotella glycoprotein augmented CD26 expression on gingival fibroblasts. Among the stimulants, IL-1
exhibited the most
potent activity. Enzymatic activity of CD26 induced by IL-1
on
fibroblasts was determined colorimetrically in terms of Gly-Pro hydrolysis of a synthetic chromogenic substrate, Gly-Pro
p-nitroanilide. Among various inhibitors tested, diprotin A
and phenylmethylsulfonyl fluoride inhibited the enzymatic activity,
suggesting that the enzyme induced by IL-1
was DPPIV. The
upregulation of CD26 mRNA expression upon stimulation with IL-1
was
also revealed by a quantitative reverse transcription-PCR assay. In the
kinetic experiment, 48 h and several days were required for
maximum CD26 mRNA accumulation and CD26 molecule expression on the cell
surface, respectively. The addition of cycloheximide at 2 h before
IL-1
stimulation almost completely inhibited the accumulation of
CD26 mRNA. These results suggested that induction of CD26 on human
gingival fibroblasts is regulated at the transcriptional level and is
also dependent on a de novo-synthesized protein factor(s).
*
Corresponding author. Mailing address: Department of
Endodontics and Periodontics, Tohoku University School of Dentistry, 4-1 Seiryo-machi, Aoba-ku, Sendai, 980-8575, Japan. Phone:
81-22-717-8336. Fax: 81-22-717-8339. E-mail:
eiji{at}mail.cc.tohoku.ac.jp.
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