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

Protease-Mediated House Dust Mite Allergen-Induced Reactive Oxygen Species Production by Neutrophils

“…However, a recent study reported conflicting data [21]. That is, although IgG and IgA each stimulated a concentration-dependent release of superoxide, anti-IgE antibodies did not induce superoxide production [21]. The results from the latter study agree with those of the present study in which we demonstrated that anti-IgE antibodies were unable to induce ROS production by neutrophils isolated from asthmatics sensitized with HDM allergens.…”

“…Anti-IgE antibodies have been shown to stimulate a superoxide-dependent induction of cyclo-oxygenase synthesis and activity in neutrophils [20]. However, a recent study reported conflicting data [21]. That is, although IgG and IgA each stimulated a concentration-dependent release of superoxide, anti-IgE antibodies did not induce superoxide production [21].…”

IL-13 overexpression in mouse lungs triggers systemic genotoxicity in peripheral blood

“…Increased level of IgE is a major factor in the etiology of asthma and is found abundantly in the serum of both human and murine models of asthma [25] [26] [27]. Therefore we assessed the levels of IgE in our transgenic IL-13 over-expression model.…”

Neutrophil-like low-density granulocytes are elevated in patients with moderate to severe persistent asthma

“…The PBMC and normal-density granulocyte fractions were isolated as described previously. 13 Briefly, venous blood was diluted 1:1 with sterile saline (Baxter, Deerfield, Illinois) containing 4 mmol/L of ethylenediaminetetraacetic acid and was centrifuged on a 3-mL cushion of Lymphocyte Separation Medium (Lonza, Walkersville, Maryland) in a 15-mL polystyrene conical centrifuge tube for 30 minutes at 300g (4 C) with the brake off. The PBMCs were carefully collected by aspiration from the plasmaelymphocyte separation medium interface, diluted 1:3 with sterile saline, and centrifuged for 10 minutes at 250g (4 C).…”

“…Normal-density granulocytes (neutrophils and eosinophils) were isolated from the granulocyteeerythrocyte pellet by 3 cycles of brief hypotonic lysis as described previously. 13 The PBMCs and granulocytes were suspended in RPMI-1640 for cell counting and then analyzed immediately by flow cytometry. Cytospin preparations of the normal-density granulocytes were prepared and treated with Wright-Giemsa stain to quantify the percentage of eosinophils, which was determined by counting at least 200 cells.…”