ABSTRACT
The present study was undertaken to investigate the effect of human PMNs on the production of TNF-α by the human peripheral blood mononuclear cells (PBMCs) and to elucidate its tentative mechanism. Human PMNs and PBMCs were isolated from the venous blood of healthy donors by dextran sedimentation and density gradient centrifugation. In the presence of lipopolysaccharide (LPS), PMNs and PBMCs were cocultured at the ratio of 2:1 for 20 h and the concentration of TNF-α in the supernatant was measured by enzyme-linked immunosorbent assay. The binding rate of monocytes with the fluorescein isothiocyanate-labeled LPS (FITC-LPS) and the mean surface fluorescence intensity of monocytes were analyzed by flow cytometry. Results showed that PMNs were capable of inhibiting the TNF-α release from PBMCs (P＜0.05). PMNs suppressed the TNF-α release from PBMCs by 45% on average when PMNs and PBMCs cocultured at the ratio of 2:1. Paraformaldehyde-fixed PMNs still demonstrated the same inhibition (P＜0.05)，which proved that the inhibition was dependent on cell-to-cell contact and suggested that effector molecules responsible for this effect existed on the cell surface of PMNs. In the presence of PMNs, the binding rate of monocytes with the FITC-LPS and the mean surface fluorescence intensity of monocytes were not affected compared with PBMCs alone (P＞0.05). As incubation time was prolonged, the binding of FITC-LPS to monocytes increased (P＜0.05). Thus PMNs did not block the binding of LPS with monocytes. It was concluded that PMNs suppressed the TNF-α release from PBMCs via cell-to-cell interaction. In a cell-contact dependent manner, PMNs might interfere with the signal transduction pathway through which LPS activated PBMCs, thus attenuating the response of PBMCs to LPS and downregulating the TNF-α release.
ABSTRACT
AIM: To study the relationship between prostaglandins and acute pulpitis. METHODS: Rat traumatic pulpitis model was established by pulp exposure. The kinetic pathological changes in dental pulpal tissues and changes of PGE 2?6-Keto-PGF 1? and TXB 2 concentration in dental pulp were observed. RESULTS: After pulpal trauma, the dental pulp showed inflammatory changes and the concentrations of PGE 2?6-Keto-PGF 1? and TXB 2 were increased, which peaked at 6 hour post-trauma. CONCLUSION: Prostaglandins play a significant role in the pathogenesis of pulpitis.
ABSTRACT
AIM: To investigate the effect of human polymorphonuclear leukocytes (PMNs) on the release of TNF-? by the human peripheral blood mononuclear cells (PBMCs) and to elucidate its mechanism. METHODS: Human PMNs and PBMCs were isolated from the venous blood of healthy donors by dextran sedimentation and density gradient centrifugation. After the cells were cocultured at the ratio of 2:1 in the presence of lipopolysaccharide (LPS), the concentration of TNF-? in the supernatant was measured by enzyme-linked immunosorbent assay. The binding rate of monocytes with the fluorescein isothiocyanate-labeled LPS (FITC-LPS) and the mean surface fluorescence intensity of monocytes were analyzed by flow cytometry. RESULTS: PMNs do not produce detectable TNF-? in the presence of LPS. PMNs were capable of inhibiting the TNF-? release from PBMCs ( P