The present study was undertaken to investigate theeffect of human PMNs on the production of TNF-α by the human peripheral blood mononuclearcells (PBMCs) and to elucidate its tentative mechanism. Human PMNs and PBMCs were isolatedfrom the venous blood of healthy donors by dextran sedimentation and density gradientcentrifugation. In the presence of lipopolysaccharide (LPS), PMNs and PBMCs werecocultured at the ratio of 2∶1 for 20 h and the concentration of TNF-α in thesupernatant was measured by enzyme-linked immunosorbent assay. The binding rate ofmonocytes with the fluorescein isothiocyanate-labeled LPS( FITC-LPS) and the mean surfacefluorescence intensity of monocytes were analyzed by flow cytometry. Results showed thatPMNs were capable of inhibiting the TNF-α release from PBMCs (P<0.05). PMNs suppressedthe TNF-α release from PBMCs by 45% on average when PMNs and PBMCs cocultured at theration 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 thateffector molecules responsible for the effect existed on the cell surface of PMNs. In thepresence of PMNs, the binding rate of monocytes with the FITP-LPS and the mean surfacefluorescence intensity of monocytes were not affected compared with PMBCs 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 PMNssuppressed the TNF-α release from PMBCs via cell-to-cell interaction. In a cell-cotactdependent manner, PMNs might interfere with the signal transduction pathway through whichLPS activated PBMCs, thus attenuating the response of PBMCs to LPS and downregulating the TNF-α release.

* Supported by the National Natural Science Foundation ofChian (No. 39670309) (PAN Jian-bo LI Hao-wei YAN Liang YANG Hao-zhuang ZHANG Sui-me WANG Yan-ping FU Yong-me)