Factors secreted by untreated and hydrocortisone-treated monocytes that modulate neutrophil function.

When incubated for 1.0 hr with neutrophils isolated from bovine peripheral blood, hydrocortisone (0.05, 0.5, or 5.0 micrograms/ml) had no significant effect on their ability to ingest Staphylococcus aureus, to reduce nitroblue tetrazolium (NBT) or iodinate protein, or to mediate antibody-dependent cell-mediated cytotoxicity (ADCC) against chicken erythrocytes. Random migration was significantly enhanced by the highest concentration of hydrocortisone (HC) but was unaffected by the lower concentrations. Resting bovine monocytes were incubated for 24 hr in medium with or without added hydrocortisone (0.05, 0.5, or 5.0 micrograms/ml). Purified bovine neutrophils were then incubated for 1.0 hr with the resulting monocyte supernatant (MS). The MS from untreated monocytes significantly enhanced neutrophil ADCC but did not affect the other neutrophil functions evaluated. Supernatants from monocytes incubated with 0.5 or 5.0 micrograms/ml hydrocortisone (HC-treated MS) failed to enhance neutrophil ADCC but did enhance neutrophil random migration under agarose. The other parameters of neutrophil function were unaffected. Production of the factors in MS was reduced by inhibition of protein synthesis in monocytes. Their activity was reduced by exposure of MS to proteolytic enzymes, suggesting that the monocyte factors were polypeptides or proteins. Protein synthesis by the neutrophil was not necessary for its response to the monocyte-produced ADCC-enhancing factor but was necessary for its response to the HC-induced monocyte factor. The results suggest that the antiinflammatory effects of glucocorticoids may be partially mediated by factors released by monocytes.