Recently, we described the presence of a blocking factor (BF) in rat serum, which inhibited the histamine release from rat mast cells in vivo and in vitro. The blocking activity was demonstrated in human serum as well. Qualitative analysis of the purified preparations demonstrated a major component with an apparent molecular weight of 70,000 daltons. In human serum the blocking factor was identified as transferrin (TF) by serological and biochemical methods. BF (DEAE-peak 1) and the iron binding proteins transferrin and lactoferrin (LF) are shown to inhibit the histamine release in vitro. The dose response curves reveal that inhibition by these proteins is dependent on their degree of iron saturation. Furthermore, unlike lactoferrin, the effects of transferrin and BF (DEAE-peak 1) follow the same pattern. Their mechanism of action remains to be elucidated.
Recently, we described a factor in rat and human serum with inhibitory activity on the 2-hour passive cutaneous anaphylactic (PCA) reaction in rat skin. The Ca-ionophore-induced histamine release from rat peritoneal mast cells was inhibited as well. In human serum, inhibitory activity for the in vitro histamine release from rat mast cells was shown to be present within two serum fractions. One molecule was purified by 50–70% ammonium sulfate precipitation and subsequent DEAE chromatography at pH 5.4. The main component showed complete identity with transferrin. Commercially available transferrin was active in vitro as well. The dose-response plot revealed two inhibition maxima at transferrin concentrations of 0.05–5 ng/ml and at more than 1 mg/ml, respectively. Subsequently it was shown that the degree of iron saturation was critical for the decrease in histamine release. The mediator release in vivo (PCA) could not be inhibited by the iron transport protein. Inhibitory activity in vivo was however mediated by the second serum fraction, which was characterized by a molecular weight of approximately 150,000 daltons and an IEP within the alkaline range. These data suggest that exogenous factors may be potent modulators of inflammatory reactions.
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