EFFECT OF CAMPYLOBACTER-RECTUS LPS ON PLASMINOGEN ACTIVATOR-PLASMIN SYSTEM IN HUMAN GINGIVAL FIBROBLAST CELLS

Citation
N. Ogura et al., EFFECT OF CAMPYLOBACTER-RECTUS LPS ON PLASMINOGEN ACTIVATOR-PLASMIN SYSTEM IN HUMAN GINGIVAL FIBROBLAST CELLS, Journal of Periodontal Research, 30(2), 1995, pp. 132-140
Citations number
53
Categorie Soggetti
Dentistry,Oral Surgery & Medicine
ISSN journal
00223484
Volume
30
Issue
2
Year of publication
1995
Pages
132 - 140
Database
ISI
SICI code
0022-3484(1995)30:2<132:EOCLOP>2.0.ZU;2-E
Abstract
The plasminogen activator (PA)-plasmin system is implicated in the deg radation of the extracellular matrix in inflammation through activatio n of metalloproteases and prekallikrein. We examined the activation of the PA-plasmin system in human gingival fibroblast cells (Gin-1 cells ) following treatment with lipopolysaccharide (LPS) from Campylobacter rectus, which is frequently detected at sites of periodontal disease. The C. rectus LPS stimulated the plasmin activity in the conditioned medium of Gin-1 cells in a time- and dose-dependent manner, and C. rec tus LPS also stimulated the PA activity in the conditioned medium. The PA produced by Gin-1 cells was determined to be urokinase PA (uPA), a s preincubation of Gin-1 conditioned medium with anti-uPA antiserum co mpletely inhibited the PA activity while that with anti-tPA antiserum had no inhibitory effect. The concentration of PA inhibitor-1 (PAI-1) in the conditioned medium was decreased by the addition of C. rectus L PS. Therefore, the enhancement of plasmin activity in the conditioned medium was dependent on increased uPA activity via the decrease of the PAI-1 level of Gin-1 cells treated with C. rectus LPS. Furthermore, t he conditioned medium of Gin-1 cells treated with C. rectus LPS showed significantly increased kallikrein activity, indicating the conversio n of prekallikrein to kallikrein, which converts kininogen into kinin. These findings suggest that C. rectus LPS is a potent stimulator of i nflammation of gingival tissue which acts through stimulation of the P A-plasmin system.