Lactoferrin inhibits prostaglandin E2 secretion by breast milk macrophages.

Abstract

The interaction between human breast milk macrophages and lactoferrin (LF) in its native form was studied in in vitro culture. Competitive inhibition-binding studies with 125I-LF and unlabeled LF showed that a specific receptor for LF was present on breast milk macrophages. LF at concentrations of 10(-6) -10(-9)M resulted in a dose-dependent inhibition of prostaglandin E2 secretion by breast milk macrophages (control-45 +/- 7; LF 10(-6)M -9 +/- 1 ng/ml/10(6) cells). This inhibitory effect was also observed when the macrophages were stimulated with Concanavalin A (LF 10(-6) M -80 +/- 5; 10(-9) M -45 +/- 8% inhibition of prostaglandin E2 secretion by Concanavalin A stimulated macrophages). Lactalbumin and lactoglobulin had no effect. Similar concentrations of LF had no effect on lysozyme production. We also demonstrated that human milk macrophages are capable of eliciting an oxidative burst as measured by superoxide or hydrogen peroxide production when stimulated by phorbol myristate acetate in in vitro culture. (basal superoxide -1.4 +/- 0.3; phorbol myristate acetate 28.8 +/- 3.5 nmol/1 X 10(6) cells/90 min; basal hydrogen peroxide 11.7 +/- 4.6; phorbol myristate acetate -57.5 +/- 2.3 nmol/mg protein/90 min). LF had no effect on the oxidative burst. These results suggest that interaction of aqueous and cellular components of breast milk may occur and result in varied physiological effects.