Expression of the high affinity IgE receptor by neutrophils of individuals with allergic asthma is both minimal and insensitive to regulation by serum IgE.

Abstract

We evaluated the hypothesis that serum IgE regulates neutrophil FcepsilonRI expression in the same manner as described for other FcepsilonRI+ cells. FcepsilonRI expression by neutrophils of 40 asthma subjects and 20 control subjects did not correlate with serum IgE levels, whereas FcepsilonRI expression by basophils of the same subjects showed a highly significant correlation. The level of FcepsilonRI expression by neutrophils of both asthma and control subjects was approximately 1% of that for basophil FcepsilonRI expression. IgE+ neutrophils were minimally detectable, and FcepsilonRI alpha-subunit was not detected in Western blots of neutrophil membranes and cytosol. The neutrophil FcepsilonRI did not support anti-IgE stimulated superoxide release or IgE-induced increase in neutrophil survival. We conclude that FcepsilonRI expression by neutrophils of both asthma patients and control individuals is minimal at best and that, if present, neutrophil FcepsilonRI expression, unlike that of other human FcepsilonRI+ cells, is not regulated by serum IgE.