Effect of Campylobacter rectus LPS on plasminogen activator‐plasmin system in human gingival fibroblast cells

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Abstract
The plasminogen activator (PA)‐plasmin system is implicated in the degradation of the extracellular matrix in inflammation through activation 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. rectus LPS also stimulated the PA activity in the conditioned medium. The PA produced by Gin‐1 cells was determined to be urokinase PA (uPA), as prein‐cubation of Gin‐1 conditioned medium with anti‐uPA antiserum completely in‐hibited 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 LPS. 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, the conditioned medium of Gin‐1 cells treated with C. rectus LPS showed significantly increased kallikrein activity, indicating the conversion of prekallikrein to kallikrein, which converts kininogen into kinin. These findings suggest that C. rectus LPS is a potent stimulator of inflammation of gingival tissue which acts through stimulation of the PA‐plasmin system.