Endotoxin priming of monocytes augments Fc gamma receptor cross-linking-induced TNF-alpha and IL-1 beta release.

Cross-linking receptors for the Fc region of immunoglobulin G (IgG) (Fc gamma R) induces tumor necrosis factor-alpha (TNF-alpha) release; however, there is controversy about release of interleukin (IL)-1 beta. The purpose of this study was to investigate the role of endotoxin priming on the ability of monocytes to release these cytokines after Fc gamma R cross-linking. Monocytes were incubated with plated or soluble human IgG or albumin with or without endotoxin priming. Monocytes isolated by Percoll, containing low concentrations of endotoxin, and incubated on plated IgG released 4.5 +/- 1.6 ng/ml TNF-alpha and 1.6 +/- 0.6 ng/ml IL-1 beta. Monocytes isolated by a "clumping" technique released 1.0 +/- 0.4 ng/ml TNF-alpha but no IL-1 beta. Priming with endotoxin, which did not affect Fc gamma R expression, resulted in augmented release of TNF-alpha (4.3 +/- 1.3 vs. 0.1 +/- 0.0 ng/ml, P < 0.05) and IL-1 beta (4.0 +/- 1.0 vs. 0.6 +/- 0.3 ng/ml, P < 0.01) when clumped monocytes were incubated on plated IgG vs. plated albumin.