Activation of respiratory burst in polymorphonuclear leukocytes upon contact with stimulated T cells and inhibition by high-density lipoproteins (HDLs)

Background

Polymorphonuclear neutrophils (PMNs) are attracted early at sites of inflammation, where they are in close proximity with other types of immune cells. Cellular contact with stimulated T cells are known to prime PMNs for respiratory burst, and direct cell–cell contact between T cells and monocytes is a major mechanism that triggers the production of inflammatory cytokines.

Methods

We analysed the direct induction of the respiratory burst in human PMNs upon contact with stimulated T cells. The production of reactive oxygen species (ROS) by PMNs was monitored in vitro by the luminol-enhanced chemiluminescence assay.

Results

Membrane from PHA/PMA-stimulated human T lymphocytes and from T-cell line HUT-78 induced a dose-dependent ROS production by PMNs, demonstrating that stimulated T-cells are able to stimulate PMN respiratory burst by direct cell–cell contact. Neither TNF soluble receptors nor IL-1 receptor antagonist interfered with ROS production induced by T-cell membranes. Monoclonal antibodies directed toward CD-18 inhibited 60% of PMN respiratory burst induced by stimulated T-cell membrane, while antibodies to CD11a,b,c and CD69 had no effect. These results suggest a partial role for β-2-integrin CD18 in PMN activation. Furthermore, HDL inhibited stimulated T-cell induced PMN respiratory burst in a dose-dependent manner, allowing a complete inhibition for 200 μg/ml. Similar inhibitory effects of HDL have previously been described in activation of monocytes by direct cell–contact.

Conclusion

These results emphasize the importance of direct cell–cell contact in inflammatory processes and strongly suggest that at the surface of T cells, similar molecules, although affected by different coactivators, are involved in the activation of both monocytes–macrophages and PMNs.