Soluble CD14-dependent intercellular adhesion molecule-1 induction by Porphyromonas gingivalis lipopolysaccharide in human gingival fibroblasts

Background: Intercellular adhesion molecule-1 (ICAM-1) is involved in the a ccumulation and activation of leukocytes in inflammatory sites through bind ing to beta(2) integrins expressed on leukocytes, We investigated whether o r not lipopolysaccharide (LPS) derived from the periodontopathic bacterium Porphyromonas gingivalis affects ICAM-1 expression on human gingival fibrob lasts (HGF). CD14 is a receptor For LPS on monocytes and macrophages and is also present in serum as a soluble protein. We further examined the effect s of serum and soluble CD14 (sCD14) on ICAM-1 expression in HGF stimulated with P: gingivalis LPS. Methods: HGF were prepared from explants of human gingival tissues and incu bated in 96-well culture plates before LPS stimulation, LPS derived from Es cherichia coli O55:B5 and P. gingivalis ATCC 33277 LPS were employed. sCD14 was purified from normal human serum (NHS) by affinity chromatography usin g an anti-CD14 monoclonal antibody. ICAM-1 expression on HGF was measured b y a cell enzyme-linked immunosorbent assay. Results: P. gingivalis LPS induced ICAM-1 on HGF in a dose-dependent manner in the presence of either 10% fetal calf serum or 2% NHS. The ability of I ! gingivalis LPS to induce ICAM-1 was comparable to that of LPS from E. col i at high LPS concentrations. In the absence of NHS, ICAM-1 induction was n egligible in HGF stimulated with P. gingivalis LPS, reaching a maximum at 2 % NHS. The ICAM-1 expression induced by P. gingivalis LPS was inhibited by a monoclonal antibody to CD14. Supplementation of serum-free medium with sC D14 alone restored the capacity of HGF to respond to P gingivalis LPS. Conclusions: These results indicate that P. gingivalis LPS induces ICAM-1 e xpression in HGF-in an sCD14-dependent manner. The overexpression of ICAM-1 on fibroblasts in gingiva induced by P. gingivalis LPS seems to be involve d in the retention of inflammatory cells in periodontitis lesions.