Immunological Release Of Histamine Research Articles

H3 Receptor Expression in the Spinal Trigeminal Nucleus Caudalis in a Rat Model of Allergic Rhinitis

Background: Allergic rhinitis is one of the most frequently observed allergic diseases. Although antihistamine medication is an effective symptomatic treatment for this disease, it is not suffcient enough to improve quality of life, requiring an additional treatment. Excessive sneezing is a typical symptom of allergic rhinitis in response to immunological release of histamine, and we hypothesized that this could be due to characteristic changes on the reflex pathway, particularly a nucleus receiving nasal trigeminal afferents, the spinal trigeminal nucleus caudalis (Sp5C), via a histamine mechanism(s). In the present study, we created an allergic rhinitis model by conventional methods, harvesting brainstem tissues to perform immunohistochemistry for histamine receptor subtype 3 (H3R) in Sp5C. Methods: Male Fisher 344 rats (8 weeks old) were sensitized and nasally challenged to Ovalbumin. After the Ovalbumin challenge into the nasal cavity, the number of sneezing was visually counted for 13 min and repeated for 7 days. After that, animals were euthanized, brainstems were extracted, and immunohistochemistry were performed with various antibodies, including anti-H3R and -GFAP. In some animals, to identify the subregion within Sp5C where nasal trigeminal afferents are transmitted from the nasal mucosa, capsaicin (0.3mM), a potent nociceptive substance, was administered into the nasal cavity and then immunohistochemistry of c-Fos expression was performed. Quantitative analysis was performed by area of fluorescent staining. Results: Intranasal administration of capsaicin markedly increased c-Fos expression in Sp5C compared to non-administration control, confirming the subregion of Sp5C receiving nasal afferent information. The allergic rhinitis model rats showed a significant increase in sneezing frequency in response to Ovalbumin nasal challenge compared to non-sensitized rats challenged with Ovalbumin or saline (56.8±3.9 vs. 16.6±1.6 vs. 23.7±3.2 [sneezes during a total observation period]; p<0.001). The expression pattern of H3Rs was punctate and co-stained with GFAP in many cases. Both H3 receptor and GFAP expressions were significantly decreased in allergic model rats compared to control rats (control vs. allergic; 21.2±1.2 vs.6.4±0.5 [%] in H3Rs, p<0.001; 16.2±0.5 vs.10.9±0.8 [%] in GFAP, p<0.001). No difference in DAPI staining was observed (14.5±0.8 vs.13.7±0.5 [%], p=0.223), suggesting similar population of cells in data analyzed from both groups. Discussion: These results may suggest that Sp5C is part of the sneezing reflex pathway and that a decrease in H3Rs, including those on astrocytes, is involved in worsening clinical symptoms of allergic rhinitis such as excessive sneezing. This research was supported by KAKENHI, Grant-in-Aid for challenging Exploratory Research # 21K19182. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Modulation of the immunological response of guinea pig mast cells by carbon monoxide

Challenge of guinea pig mast cells with antigen under aerobic conditions induced the expected release of histamine and led to a significant increase in intracellular calcium ([Ca2+]i) and cyclic adenosine monophosphate (cAMP) levels. Prior exposure to CO decreased the immunological histamine release. This effect was accompanied by a decrease in the levels of [Ca2+]i and by an increase in the cyclic guanosine monophosphate (cGMP) levels. The exposure of mast cells to nitrogen (N2) did not modify the release of histamine. The CO-mediated inhibition of the immunological release of histamine was reversed by the soluble guanylate cyclase inhibitor (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, ODQ) and by oxyhaemoglobin (HbO2). Incubation of mast cells for 4 h with hemin, a heme oxygenase (HO) inducer, resulted in an increase in HO activity, measured as bilirubin production. Hemin abated the immunological release of histamine, in similar fashion to exogenous CO, and increased the cGMP levels. These effects were reversed by ODQ and HbO2. It is proposed that CO from an exogenous or endogenous source stimulates guanylyl cyclase and causes cGMP formation which then induces calcium to be sequestrated so that the [Ca2+]i concentration falls and histamine release is inhibited.

Oxatomide inhibits the release of proinflammatory mediators from human basophils and mast cells.

Oxatomide (OXA), a histamine H1 receptor antagonist, is effective in the treatment of patients with allergic rhinitis, some allergic skin disorders, and bronchial asthma. We have characterized the effect of OXA on the immunologic release of preformed (histamine and tryptase) and de novo synthesized mediators (leukotriene C4:LTC4 and prostaglandin D2:PGD2) from human basophils and mast cells purified (from 10 to 82%) from human lung parenchyma (HLMC) and skin tissue (HSMC). Preincubation (15 min, 37 degrees C) of basophils with OXA (10(-7)-10(-5) M) before Der p I antigen or anti-IgE challenge concentration-dependently (10-40%) inhibited the immunologic release of histamine and LTC4. OXA (10(-7)-10(-5) M) also inhibited (10-40%) histamine, tryptase and LTC4 release from HLMC activated by anti-IgE. In addition, OXA caused a concentration-dependent inhibition of histamine, tryptase and PGD2 release from HSMC immunologically challenged with a monoclonal antibody against the alpha chain of the high affinity receptor for IgE (anti-Fc epsilon RI) or anti-IgE. These results demonstrate that OXA exerts anti-inflammatory activities by inhibiting the release of preformed and de novo synthesized mediators from human basophils and mast cells.

Characterization of LDL and VLDL Binding Sites on Human Basophils and Mast Cells

Recent data suggest that basophils and mast cells play a potential role in the processing and accumulation of plasma lipoproteins. This study investigated the interactions of 111In-low-density lipoprotein (LDL), 111In-acetyl-LDL, and 111In-very-low-density lipoprotein (VLDL) with purified primary human blood basophils, immortalized human basophils (KU812 cell line), and a human mast cell line, HMC-1. Binding sites for 111In-LDL resolved into curvilinear Scatchard plots indicating two classes of specific binding sites on primary basophils (Bmax1, 7404 sites/cell; Kd1, 1.9 nmol/L; Bmax2, 39,611 sites/cell; Kd2, 29 nmol/L), on KU812 cells (Bmax1, 8290 +/- 2690 sites/cell; Kd1, 2.4 +/- 0.6 nmol/L; Bmax2, 46,470 sites/cell; Kd2, 33.4 +/- 7.8 nmol/L), and on HMC-1 cells (Bmax1, 7840 +/- 360 sites/cell; Kd1, 1.8 +/- 0.8 nmol/L; Bmax2, 61,450 +/- 9900 sites/cell; Kd2, 28.4 +/- 9.4 nmol/L). On KU812 cells, binding of 111In-LDL was displaced by apolipoprotein (apo)-E-rich high-density lipoprotein (HDL) (IC50, 14 +/- 6 nmol/L), LDL (IC50, 29 +/- 11 nmol/L), VLDL (IC50, 55 +/- 21 nmol/L), HDL2 (IC50, 420 +/- 140 nmol/L), and heparin (IC50, 67 +/- 28 nmol/L), whereas no competition was produced by HDL, HDL3, or acetyl-LDL (IC50, > 1 mumol/L). Western blot analysis using the monoclonal antibody C7 confirmed the presence of the LDL receptor on human basophils and HMC-1 cells. 111In-acetyl-LDL binding sites (scavenger receptor) could be detected neither on human basophils nor on HMC-1 cells. 111In-VLDL bound to a single class of high-affinity binding sites on primary basophils (Bmax, 4320 sites/cell; Kd, 10 nmol/L), KU812 cells (Bmax, 4020 +/- 840 sites/cell; Kd, 8 +/- 3 nmol/L), and HMC-1 cells (Bmax, 6143 +/- 1866 sites/cell; Kd, 4 +/- 2 nmol/L). 111In-VLDL binding was displaced by VLDL > LDL > apoE-rich HDL but not by heparin (IC50 > 1 mmol/L). In the presence of prostaglandin E1, the number of 111In-LDL receptors increased by 150% (P < .05) in the high-affinity range and by 170% (P < .01) in the low-affinity range, whereas the number of 111In-VLDL binding sites remained unchanged. VLDL, LDL, HDL, and the subclasses HDL2 and HDL3 inhibited immunological histamine release by primary normal basophils (n = 3) and mast cells (n = 3). Our results provide evidence for the existence of LDL and VLDL binding sites on human basophils and HMC-1 mast cells. The exact biological and pathophysiological roles of these sites remain to be elucidated.

Nitroprusside, a nitrogen oxide generating drug, inhibits release of histamine and tryptase from human skin mast cells

We have investigated the effects of the nitric oxide donor sodium nitroprusside on the immunologic release of histamine and tryptase from human mast cells. Isolated human skin mast cells were purified using Percoll gradient centrifugation. Mast cells with a purity of 70–90% were preincubated for 30 minutes with sodium nitroprusside and subsequently stimulated with anti-IgE. Upon challenge with anti-IgE, a release of 6.37±0.46 nmol histamine and 612±49 ng tryptase per 106 cells was observed. In presence of sodium nitroprusside a dose-dependent decrease of the release occurred. The results suggest that nitric oxide is effective in reducing the release of histamine and tryptase from human skin mast cells.

New pharmacological profiles of loratadine: Effects on platelet aggregation and histamine release from repository cells

Loratadine is endowed with antiallergic activity. It reduces both the immunological release of histamine in active anaphylaxis of isolated guinea-pig mast cells and in anti-IgE challenged human basophils as well as the non-immunological release of histamine induced by compound 48/80 and calcium ionophore A 23187 in isolated purified rat serosal mast cells. Loratadine was also found capable of directly reducing platelet aggregation induced by different agonists in a concentration-dependent fashion. It is capable of blocking the potentiation afforded by histamine on human platelet aggregation induced by thrombin, collagen and arachidonic acid. The present results suggest a broader profile for loratadine beyond its original role as a non-sedative anti-H1-antihistaminic drug.

Effect of astemizole on antigen-mediated histamine release from the blood of patients with allergic rhinitis.

The main objective of this study was to test the effectiveness of astemizole in vitro in blocking the release of histamine from blood of patients with allergic rhinitis. The results of this investigation indicated that astemizole inhibited allergen-mediated histamine release from blood basophils of patients with this allergic disorder. The inhibition by astemizole (33-156 mumol) was immediate, requiring no pre-incubation of the cells, and was dose-dependent, with maximal inhibition of about 91%. The relatively high potency of astemizole in inhibiting the immunologic release of histamine may provide an additional measure in the treatment of allergic rhinitis with this H1-receptor antagonist.

LY 186655, a phosphodiesterase inhibitor, inhibits histamine release from human basophils, lung and skin fragments

LY 186655 (Tibenelast, Lilly) is a new phosphodiesterase inhibitor, not derived from the xanthine, possessing bronchodilating activity in animals. The aim of this work was to study the effect of LY 186655 and theophylline on histamine release from human leukocytes, skin and lung fragments. Histamine was measured using a spectrofluorometric method. Both drugs (3 × 10 −5 −3 × 10 −3M) exhibited a dose-dependent inhibition on anti-IgE (1/2000)-induced histamine release from human leukocytes. At 3 × 10 −3M, theophylline was significantly more effective than LY 186655 (mean inhibition 94 and 42%, respectively). On lung fragments, theophylline and LY 186655 (3 × 10 −5 −3 × 10 −3M) caused strong and comparable inhibitory effects on anti-IgE (1/500)-induced histamine release with a mean inhibition reaching maximally 65%. Histamine release induced by compound 48/80 (1 mg/ml) on sliced human foreskin was reduced with both drugs (3 × 10 −3M) by about 37%. We conclude that LY 186655 inhibits in vitro immunological histamine release from human lung and cutaneous mast cells as well as basophils with a similar pattern of activity to theophylline.

Nimesulide, a Nonsteroidal Anti-Inflammatory Drug, Displays Antianaphylactic and Antihistaminic Activity in Guinea-Pigs

The nonsteroidal anti-inflammatory compound nimesulide (4-nitro-2-phenoxymethane sulfonanilide) antagonises the effect of histamine and inhibits the release of this autacoid during immunological reaction in guinea-pigs. The antihistaminic activity of nimesulide, studied in isolated guinea-pig trachea, is specific for the H1-receptor and is of a noncompetitive type. At a concentration of 1 × 10−5 mol/L, the potency of nimesulide is nearly half that of mepyramine (pyrilamine) at 1 × 10−6 mol/L. Furthermore, unlike indomethacin, nimesulide dose-dependently antagonises the effect of histamine on airway resistance of anaesthetised guinea-pigs. In actively ovalbumin-sensitised anaesthetised guinea-pigs, both nimesulide and indomethacin significantly protected the animals from the fatal systemic anaphylactic crisis. However, in perfused sensitised guinea-pig lungs, nimesulide reduced the anaphylactic release of histamine in a concentration-dependent way, whereas indomethacin, in spite of its inhibitory potency on thromboxane A2 formation, potentiated the immune release of histamine. The bronchoconstriction induced by acetaldehyde, administered by aerosol (2.5% in saline) in sensitised anaesthetised guinea-pigs, was substantially reduced by both nimesulide and mepyramine administered by inhalation and by intravenous injection. These data further support the antihistaminic property of nimesulide and also suggest a possible interference of the compound with the degranulation process of sensitised mast cells in response to acetaldehyde. In conclusion, the capacity of nimesulide to control the immunological release of histamine and to attenuate its effect at the receptor level of the airway smooth muscles of the guinea-pig, may have some therapeutic relevance in patients with inflammation of the respiratory tract aggravated by intolerance to aspirin-like drugs.

Immune release of histamine and other lipid mediators from guinea-pig isolated kidney: Antagonism by BN-52021

The ability of a specific PAF-receptor antagonist, BN-52021, to control the release of mediators of anaphylaxis from actively sensitized (ovalbumin) guinea-pig has been investigated "in vitro". BN-52021 perfused through the kidney at different molar concentrations (1 x 10(-4)-1 x 10(-5)-1 x 10(-6] prior to antigen challenge neither modified the basal values of perfusion pressure nor stimulated mediator release from the organ. On the contrary, the compound antagonized in a concentration dependent way both vasoconstriction of the renal vessels and the increase in the perfusate of histamine, TXB2 and SRS-A due to antigenic shock. The antagonistic activity of BN-52021 was very consistent at 1 x 10(-4) M at which concentration the immunological release of histamine and TXB2 was reduced by 75%. The beneficial effect of BN-52021 in experimental anaphylaxis of the kidney may have some therapeutic implications principally in those pathological conditions where an abnormal increase of renal histamine and other mediators may compromise the haemodynamic function of this organ.

Pharmacological activity of bamifylline on lung anaphylaxis: In vitro studies

Bamifylline, a 7–8 disubstituted theophylline derivative, reduces in a dose dependent way (1 × 10 −5 m, 1 × 10 −4 m and 1 × 10 −3 m) the release of histamine, TXB 2 (measured also as TXA 2-like material) and SRS -A (as LTD 4 like material) during the immunological challenge of actively sensitized guinea-pig lungs perfused in vitro. Theophylline was significantly less potent than bamifylline and particularly, at the higher concentrations used (1 × 10 −3 m), bamifylline was 2 · 7 times more potent than theophylline in reducing the immunological release of histamine and 1 · 6 and 1 · 5 times more potent in inhibiting the production of TXB 2 and SRS-A, respectively. These data suggest that the ability of the two xanthine derivatives to control the immunological release of histamine represents an important point in understanding the mechanism of their anti-anaphylactic activity.

The effect of azelastine on neutrophil and eosinophil generation of superoxide

Azelastine is a new investigational drug used to treat rhinitis and asthma. In addition to described actions that include inhibition of immunologic release of histamine from mast cells and basophils, blockade of smooth muscle contraction to various spasmogenic mediators, and relaxation of airway smooth muscle, azelastine has been ascribed anti-inflammatory properties. To understand further the mechanisms by which azelastine may regulate inflammation, its effect on neutrophil and eosinophil superoxide (O 2 -) generation was evaluated. Purified suspension of neutrophils (>95% pure) and eosinophils (>85% pure) were isolated from human peripheral blood samples by continuous density gradients of Percoll. The isolated granulocyte suspensions (1 × 10 5 cells) were added to 96-well microtiter plates in the presence of cytochrome c, activated by either N-formyl-methionyl-leucyl-phenylalanine, phorphol myristate actetate, calcium ionophore A23187, or opsonized zymosan particles; O 2 - generation was measured by the reduction of cytochrome c. We found that azelastine significantly inhibited both neutrophil and eosinophil generation of O 2 - in a dose-dependent fashion (10 −7 to 10 −5 mol/L) with each activator except zymosan. Furthermore, the degree to which azelastine suppressed O 2 - was similar in neutrophils and eosinophils. Thus, azelastine, in concentrations achieved therapeutically, inhibited granulocyte generation of O 2 -. This anti-inflammatory effect may also be beneficial in the treatment of asthma.

Effects of Sodium Cromoglycate and Nedocromil Sodium on Histamine Secretion from Mast Cells from Various Locations

Nedocromil sodium and sodium cromoglycate inhibited histamine release from rat peritoneal mast cells. Tachyphylaxis was observed with both drugs. The 2 compounds were extremely selective in their action, being less active against peritoneal mast cells from the hamster and completely ineffective against mast cells from the mouse. Human basophil leucocytes, tissue mast cells of the guinea-pig and rat intestinal mast cells were also unresponsive. Both drugs inhibited immunological histamine release from human pulmonary mast cells obtained by bronchoalveolar lavage (BAL) and, less effectively, from lung parenchyma. Nedocromil sodium was about 1 order of magnitude more potent than sodium cromoglycate in each case. Tachyphylaxis was observed with the dispersed lung, but not with the cells obtained by BAL, and the degree of inhibition varied inversely with the magnitude of the secretory response. The possible clinical significance of these observations is discussed.

Pathophysiological significance of the distribution of histamine receptor sub-types: a proposed dual role for histamine in inflammation and Type I hypersensitivity reactions

The pathophysiological significance of histaminergic receptors located on the membranes of immunocompetent cells is reviewed. H2-receptor agonists decrease the immunological histamine release from isolated serosal mast cells and from isolated hearts taken from actively sensitised guinea-pigs. Histamine and H2-receptor agonists inhibit the generation of superoxide anion from human neutrophils activated by FMLP and by substance P. These observations lend further support to the hypothesis of an immunodepression exerted by the activation of H2-receptors, which can be converted to immunostimulation by treatment with H2-receptor antagonists.

The Effect of Indomethacin on Immunologic Release of Histamine and Sulfidopeptide Leukotrienes from Human Bronchus and Lung Parenchyma

We studied the effect of indomethacin on immunologic mediator release from human bronchial tissue (n = 6) and lung parenchyma (n = 7). Tissues were obtained from surgical specimens, minced, passively sensitized, and challenged with antigen E or anti-IgE in the presence or absence of indomethacin. At maximal levels of immunologic stimulation with either antigen or anti-IgE, the bronchial and parenchymal tissues released approximately 5 and 20% of total histamine (net), respectively, and approximately 3.5 and 45 ng/g of immunoreactive sulfidopeptide leukotriene, respectively. Analysis by high performance liquid chromatography followed by radioimmunoassay revealed that the airway supernatants contained LTD4 and LTE4, whereas the lung parenchymal samples contained predominantly LTE4. Little or no LTC4 was detected in either airway or parenchymal samples. Incubation with indomethacin (5 x 10(-6) M) resulted in approximately a 3-fold increase in antigen or anti-IgE-induced release of leukotrienes from the bronchial tissue. Indomethacin also enhanced antigen-induced histamine release approximately 2-fold but had no effect on anti-IgE-induced histamine release from this tissue. In contrast, indomethacin had no effect on antigen or anti-IgE-induced histamine or leukotriene release from the lung parenchymal tissue at any level of immunologic stimulation. These results support the hypothesis that indomethacin enhances human anaphylactic bronchospasm in vitro through an increase in mediator release from bronchial mast cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of lysophosphatidylserine on immunological histamine release

The effect of lysophosphatidylserine on immunological histamine release has been studied in rat peritoneal mast cells actively sensitized with horse serum and in human basophils challenged with anti-IgE. In contrast to other lysophospholipids, lysophosphatidylserine enhances the immunological histamine release in rat mast cells. The effect shows the kinetics of a saturable process with an apparent K m for lysophosphatidylserine of 0.26 μM. A similar K m value (0.21 μM) is found when measuring the non-immunological histamine release activated by lysophosphatidylserine plus nerve growth factor. A comparison with phosphatidylserine shows that a half-maximal response to lysophosphatidylserine occurs at a concentration 4-times lower. In addition, the magnitude of the response is higher. At variance with rat mast cells, lysophosphatidylserine does not influence the histamine release elicited by immunological and non-immunological stimuli in human basophils. The histamine secretion in these cells is instead affected by a calcium ionophore or tetradecanoylphorbolacetate, a compound producing activation of protein kinase C.

受身皮膚アナフィラキシーモデルにおけるＫＰ‐１３６のアレルギー反応抑制作用

The pharmacological properties of KP-136 were studied using cutaneous reactions in rats and guinea pigs. KP-136 remarkably inhibited the passive cutaneous anaphylaxis (PCA) with intravenous and oral dosing. However, the inhibitory effect of KP-136 had an apparent species difference. Thus, KP-136 was more effective on rat PCA than that of guinea pig. In four rat cutaneous reactions produced by three allergic reactions and compound 48/80, KP-136 was remarkably effective on two homologous PCA induced by IgE and IgGa. The intravenous and oral doses for 50% inhibition on the PCA were 0.2 mg/kg to 0.4 mg/kg and 0.5 mg/kg to 0.9 mg/kg, respectively. KP-136 was scarcely effective on cutaneous reactions elicited by intradermal injection of histamine and serotonin which are main chemical mediators in rat homologous PCA. However, KP-136 blocked the degranulation of mast cells and decrease of histamine content in skin elicited by the PCA. In addition, KP-136 showed a potent inhibition on the immunological release of histamine from rat peritoneal exudate cells. The concentration for 50% inhibition on the histamine release was 5 ng/ml. These findings indicate that KP-136 is an oral potent inhibitor on PCA, and it acts by blocking the release of chemical mediator(s) from mast cells.

Immunologic and nonimmunologic responsiveness in ragweed-sensitized dogs

The relationship between airway responsiveness to inhaled antigen and histamine, immunologic release of lung histamine, immunologic responsiveness of skin, and specific immunoglobulin E (IgE) antibodies were examined in 11 inbred allergic dogs immunized with extracts of ragweed and grass and 5 nonimmunized control dogs from the same colony. Airway responsiveness to antigen and histamine was characterized by the doses that increased the airflow resistance of the total respiratory system to twice the control values (ED200). Highly significant correlations were found between airway responsiveness and cutaneous responsiveness to antigen and other immunologic characteristics (e.g., IgE and histamine released from lung by inhaled antigen) in all dogs. In ragweed-sensitized dogs, there was an inverse correlation between immunologic responsiveness (reflected by the cutaneous response to antigen and histamine released from lung by inhaled antigen) and nonimmunologic responsiveness of airways (histamine ED200: r = 0.73, P less than 0.05 and r = 0.75, P less than 0.01, respectively). Antigen ED200 was also correlated with histamine release from lung after antigen inhalation (r = 0.74; P less than 0.01). We conclude that airway reactions to inhaled antigen in allergic dogs are dependent not only on immunologic factors but also on the degree of nonimmunologic airway responsiveness to histamine and that these factors are correlated inversely.

Enhanced basophil histamine release to concanavalin A in allergic rhinitis

It has been suggested that IgE-dependent basophil histamine release (HR) does not necessarily relate to the amount of cell-bound IgE and, therefore, basophil “releasability” must be considered an important factor in this secretory process. To compare an IgE-dependent basophil HR process in nonatopic subjects and patients with allergic rhinitis, concanavalin A (Con A) was used as a secretagogue to stimulate mediator secretion. In 1.0 mmol/L of calcium-containing buffer, basophil HR to Con A (3.0 meg/ml) was 50.2 ± 8.6% in patients with allergic rhinitis and only 10.1 ± 3.9% in nonatopic subjects. To evaluate whether this enhanced HR might he related to increased membrane influx of calcium, the following strategy was followed. Strontium (3.0 and 10.0 mmol/L) enhances immunologic (IgE) release of basophil histamine. Although the mechanism for strontium enhancement is not established, strontium may pass through the membrane channel more easily than calcium to increase secretion. We reasoned that if the enhanced release of histamine to Con A was related to increased membrane permeability to calcium, stimulation of basophil histamine secretion in the presence of strontium would reduce this difference. In both nonatopic subjects and patients with allergic rhinitis, strontium (3.0 and 10.0 mmol/L) enhanced HR. Enhanced HR with strontium was greater with basophils from normal subjects than from subjects with allergic rhinitis. Whether our observations with strontium indicate that the enhanced histamine releasability to Con A in subjects with allergic rhinitis may, in part, be due to a greater influx of calcium after immunologic stimulation must await characterization of the strontium effect or direct measurements of calcium ion disposition. Nevertheless, these data are evidence for the phenomenon of enhanced basophil releasability in subjects with allergic rhinitis.

Immunologic histamine release from isolated human basophils during specific immunotherapy

Anti-IgE- and antigen-induced histamine release from basophils isolated from 20 atopic patients sensitive to grass pollen allergens was evaluated. The studies were made before and after short-term immunotherapy with Pollinex. It was shown, that after hyposensitization a significant decrease on anti-IgE and specific antigen-induced histamine release from basophils occurs.