Characterization of cellular response to thiol-modified gold surfaces implanted in mouse peritoneal cavity.

The early inflammatory reaction in vivo to three well defined surfaces-gold, gold coated with glutathione (GSH), and 3-mercapto-1, 2-propanediol (MG)-was assessed as manifested by the adherence and activation of inflammatory cells during implantation intraperitoneally in mice. Evaluation of cell adhesion and activation was done by immunohistochemistry using specific monoclonal antibodies directed against cell differentiation antigens CD11b/CD18, CD74, and CD25 or by measurement by chemoluminescence of reactive oxygen radical species produced by adhering cells. Cell recruitment and activation was slow on the GSH-coated gold surfaces. These surfaces also had the highest percentage of adhering cells with an intact cell membrane. The MG-coated surfaces, on the other hand, rapidly recruited and activated cells and also caused cell membrane leakage to propidium iodide, suggesting cell membrane damage or cell death. The respiratory burst of adhering cells was stimulated by phorbol-myristate acetate on the GSH-coated surface but not on the MG-coated surface and by opsonized zymosan on the Mg-coated surface but only to a small degree on the GSH-coated surface. The respiratory burst following zymosan activation of cells adhering to the MG-coated surface was inhibited by treatment with 2. 3-diphosphoglycerate, a phospholipase D inhibitor. The presented data suggest that peritoneal leukocytes adhering to foreign materials may raise a respiratory burst response via a phospholipase D-dependent and protein kinase C-independent pathway.