Free peripheral sulfhydryl groups, CD11/CD18 integrins, and calcium are required in the cadmium and nickel enhancement of human-polymorphonuclear leukocyte adherence.

Cadmium and nickel stimulate the early spontaneous adherence of peripheral human polymorphonuclear leukocytes (PMNs). Formyl-methionylleucylphenylalanine (fMLP) at 0.25 nM inhibited the PMN adherence but was stimulated at 10 or 100 nM. Cadmium or nickel, nullified the FMLP inhibitory effect, and enhanced the adherence. No clear additive effect was noticed for either metal with fMLP. Blockade of CD11/CD18 receptors abolished the adherence modulatory effect of both fMLP and metals. p-Chloromercuriphenyl sulfonate (PCMPS), at a concentration that blocks peripheral SH groups, did not affect spontaneous adherence, but completely prevented the adherence enhancement caused by cadmium or nickel. Removal of extracellular calcium diminished both the spontaneous and the metal-stimulated adherence. Ryanodine, at a concentration that persistently inactivates ryanodine-sensitive intracellular channels, inhibited spontaneous PMN adherence, but had no effect on the cadmium or nickel induced adherence enhancement. Therefore, the results indicate that cadmium and nickel adherence stimulation depends on constitutive peripheral SH groups, CD11/CD18 integrins and extracellular calcium, but not on intracellular stored-calcium release through ryanodine-sensitive channels (RyRS). In contrast, spontaneous adherence greatly depends on the release of stored calcium through RyRs, and only slightly on extracellular calcium.