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At least 19 recordsLinked to original sources
PubMed1988

Role of cyclic AMP during histamine release. Histamine release is not directly related to increase in cyclic AMP levels in rat mast cells activated by concanavalin A, anti-IgE, antigen, prostaglandin D2 and isoproterenol.

Activation of mast cells by bridging of IgE-receptors or concanavalin A (Con A) results in a rapid initial rise and fall in cyclic AMP (cAMP) levels followed by a second rise in cAMP levels and histamine release (Sullivan, T. et al. (1976) J. Immunol. 117, 713-716; Lewis, R.A. et al. (1979) J. Immunol. 123, 1663-1668; Ishizaka, T. et al. (1981) Proc. Natl. Acad. Sci. U.S.A. 78, 6812-6816). trans-4-Guanidinomethylcyclohexanecarboxylic acid 4-tert-butylphenyl ester (GMCHA-OPhBut), a strong trypsin inhibitor and an anti-allergic agent (Muramatu, M. et al. (1982) Hoppe-Seyler's Z. Physiol. Chem. 363, 203-211; Takei, M. et al. Agents Actions, in press), strongly and dose-dependently inhibited the initial and second rises in cAMP levels, and release of histamine from rat mast cells by Con A, anti-IgE and antigen. Addition of GMCHA-OPhBut after the initial rise in cAMP inhibited the second rise in cAMP and histamine release. These results suggested a possible participation of a trypsin-like proteinase, probably pH 7 tryptase present in rat mast cells, in the activation of adenylate cyclase by the above secretagogues, and the initial rise in cAMP was not directly related to the latter events. The second rise in cAMP is induced by prostaglandin D2 (PGD2), a metabolic product of arachidonic acid. PGD2 elevated the cAMP levels in mast cells whereas no histamine was secreted. GMCHA-OPhBut did not inhibit the increase in cAMP by PGD2. Therefore, the strong inhibitory effect of GMCHA-OPhBut on the second rise in cAMP might depend on the inhibition of an earlier process than the activation of adenylate cyclase by PGD2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Endotoxins release histamine by complement activation and potentiate bacteria-induced histamine release.

The histamine-releasing capability of bacterial lipopolysaccharides (LPS) was examined in human leukocyte suspensions. LPS alone did not release histamine, but it was found to enhance the histamine release caused by bacteria in basophils from persons sensitized to these bacteria. In the presence of serum, LPS was able to release histamine through complement activation. It is speculated that endotoxins reinforce release of histamine caused by bacteria in persons sensitized to these microorganisms, and a direct mediator release via complement activation might play a role in septic conditions.

Bacteria↗
PubMed1991

The stimuli releasing histamine from murine bone marrow-derived mast cells. 2. Mechanisms involved in histamine release induced by extracellular ATP and its metabolites.

Extracellular ATP stimulated histamine release and generation of leukotrience C4 (LTC4) accompanied with the formation of inositol phosphates and a rapid increase in intracellular Ca2+ ([Ca2+]i) in mouse bone marrow-derived cultured mast cells (BMMC). The rank order of histamine-releasing potency of ATP and its metabolites is ATP greater than ADP greater than AMP greater than adenosine. Nonhydrolyzable ATP analog, adenosine-5'-O-[2-thiotriphosphate] (ATP-S) released more histamine from the cells than ATP. On the other hand, simultaneous addition of adenosine analogues at micromolar concentrations potentiated histamine release from the cells induced by ATP (50 microM) or DNP-HSA antigen (0.1 ng/ml) in the following rank order: adenosine greater than AMP much greater than ADP = ATP. Histamine release potentiated by adenosine was blocked by the treatment with pertussis toxin, whereas histamine release induced by ATP was not affected by the toxin, suggesting that extracellular ATP stimulate histamine release from BMMC probably via mechanisms independent of the potentiation of histamine release induced by adenosine.

Adenosine↗
PubMed1973

Histamine release induced by human leukocyte lysates. Reabsorption of previously released histamine after exposure to cyclic amp-active agents.

The role of cyclic AMP in histamine release induced by human leukocyte lysates was investigated. Leukocytes were incubated with leukocyte lysates prepared by ultrasonic disruption, and histamine was determined fluorimetrically. Several cyclic AMP-active agents had a marked inhibitory effect on histamine release. Theophylline and isoproterenol produced 50% inhibition at concentrations of less than 10(-5) M. Prostaglandin E(1) and dibutyryl cyclic AMP inhibited release by 50% at 7 x 10(-8) M and 6 x 10(-5) M concentrations, respectively. Histamine, which has recently been shown to increase leukocyte cyclic AMP, had a pronounced inhibitory effect on lysate-induced histamine release, producing 50% inhibition at a concentration of only 2.5 x 10(-12) M.Leukocytes, incubated with leukocyte lysates, were sampled at various times and assayed for free histamine released into the incubation mixture supernates, and for bound histamine associated with the leukocyte buttons after centrifugation. Theophylline, prostaglandin E(1) and dibutyryl cyclic AMP not only blocked histamine release, but also caused a progressive decrease in free histamine when added at any time up to 30 min after initiation of the release reaction. As the free histamine decreased after addition of the inhibitors, there was a corresponding increase in the bound histamine, suggesting that previously released histamine was reabsorbed by the leukocytes after exposure to cyclic AMP-active agents. Continued incubation of leukocytes in their own histamine after completion of the release reaction also resulted in reabsorption of the previously released histamine. Previous studies have indicated that cyclic AMP inhibits leukocyte histamine release. The results of the present studies suggest that cyclic AMP modulates histamine release induced by human leukocyte lysates by stimulating reabsorption of histamine from the extracellular environment. These studies also suggest that previously released extracellular histamine may stimulate its own reabsorption by increasing the intracellular level of cyclic AMP.

Absorption↗
PubMed1995

Haemophilus influenzae release histamine and enhance histamine release from human bronchoalveolar cells. Examination of patients with chronic bronchitis and controls.

Haemophilus influenzae (H. influenzae), Streptococcus pneumoniae (S. pneumoniae) and Branhamella catarrhalis (B. catarrhalis) are often found in the lower respiratory tract of patients with chronic bronchitis. Earlier studies have shown that bacteria induce mediator release from human basophils and parenchymal lung mast cells. In this study the capability of bacteria to trigger or potentiate histamine release from superficially located mast cells in the airway epithelium was studied in cell suspensions obtained by bronchoalveolar lavage in patients with chronic bronchitis (CB). In approximately half of the patients H. influenzae and Staphylococcus aureus (S. aureus) were found to trigger histamine release, whereas no response was obtained by S. pneumoniae or B. catarrhalis. The mediator release was caused by a non-IgE-dependent mechanism. At lower concentrations of H. influenzae causing no histamine release the bacterium was found to enhance IgE-mediated histamine release triggered by anti-IgE antibody. The synergy was more pronounced in patients with CB than in controls. Since H. influenzae is found in the lower respiratory tract of the patients but not in normal individuals, the infection here may via histamine release lead to harmful effects on the airways of importance for precipitation and exacerbation of chronic bronchitis.

Adult↗
PubMed1996

Comparative ultrastructural morphology of human basophils stimulated to release histamine by anti-IgE, recombinant IgE-dependent histamine-releasing factor, or monocyte chemotactic protein-1.

An ultrastructural analysis of human basophils stimulated with anti-IgE, recombinant histamine-releasing factor (rHRF), or monocyte chemotactic protein-1 (MCP-1) (compared with unstimulated cells) was performed. Partially purified peripheral blood basophils were prepared for electron microscopy at time points known to precede histamine release and at half-maximum histamine release times for each secretagogue. Activation morphologies associated with stimulation included granule-vesicle attachments, piecemeal degranulation, anaphylactic degranulation, and uropod formation. These features were qualitatively similar in the stimulated samples. Quantitative differences were evident, however, when stimulated samples were compared with controls or at different time points after stimulation with a single agent or when individual secretagogues were compared. All stimulated samples differed quantitatively from the control samples. Rank orders for morphologic activation events revealed that the most effective trigger for anaphylactic degranulation was anti-IgE > MCP-1 > rHRF, whereas the most effective trigger for uropod formation was rHRF > anti-IgE > MCP-1. Rank orders for piecemeal degranulation and granule-vesicle attachments were the same: MCP-1 > anti-IgE > rHRF. Important relationships among these anatomic events reveal that the development of motile configurations is not associated with the development of secretion morphologies and that piecemeal degranulation precedes and is inversely related to anaphylactic degranulation in stimulated samples.

Antibodies, Anti-Idiotypic↗
PubMed1992

The stimuli releasing histamine from murine bone marrow-derived mast cells (BMMC). 3. Effect of coculture with 3T3 fibroblasts on the histamine releasability of BMMC.

Murine bone marrow-derived mast cells at 3 wk in culture were further cultured in the absence (N-BMMC) or presence (F-BMMC) of 3T3 fibroblasts in the medium containing LI-3, and were examined for their functional responses to either histamine releasing stimuli such as compound 48/80 or an inhibitor of histamine release, disodium cromoglycate. After 3 weeks in coculture with 3T3 fibroblasts, the mast cells increased their histamine content greater than 10 fold, and greater than 10% of the cells changed histochemically to become safranin positive. F-BMMC released approximately 10% histamine when challenged with compound 48/80 or substance P, whereas N-BMMC failed to do so. Furthermore, when the sensitized cells were challenged with DNP-HSA antigen, histamine release from F-BMMC but not from N-BMMC was inhibited by preincubation with disodium cromoglycate. We also examined changes in intracellular Ca2+ ([Ca2+]i) in the cells when challenged with compound 48/80. A transient increase in [Ca2+]i was observed on stimulation with the compound in F-BMMC but not in N-BMMC. Taken together, our results indicate that the interleukin 3-dependent cultured murine mast cells change functionally, as well as histochemically, into in vitro counterparts of connective tissue mast cells when cocultured with 3T3 fibroblasts and may be useful tools for analyzing the mechanisms involved in degranulation from connective tissue-type mast cells.

Animals↗
PubMed1994

[Development of the research in the field of histamine release].

Histamine release from mast cells is intimately related with degranulation. When basic histamine releasers such as compound 48/80 were applied extracellularly to isolated rat mast cells by means of microelectrophoresis, localized degranulation was evoked near the tip of micropipet in a few seconds. In response to the second electrophoretic application at the opposite side of the membrane of the same mast cells, similar local degranulation was induced. This fact clearly indicates that local degranulation does not damage mast cells to the extent of blocking following degranulation. As intracellular electrophoretic application of compound 48/80 caused a swelling of mast cell, although no degranulation was elicited. When antigen-antibody reaction was induced in a single rat mesentery mast cell by means of microelectrophoresis, the application of antigen was made extracellularly or intracellularly. At the site of extracellular application, localized degranulation and histamine release were evoked. Histamine release was evidenced by the disappearance of histamine fluorescence in the degranulated area. Neither degranulation nor histamine release was induced by intracellular application of antigen. In freeze-fracture electronmicroscopy of the resting rat mast cells, intra-membrane particles (IMPs) were randomly distributed on the plasma membrane. When sensitized cells were exposed to antigen, IMPs were markedly dispersed so as to surround bulging regions of the membrane elicited by swollen granules. As the particles gathered at the periphery of the bulges, actually no particle was seen on the protuberant region. When rat mast cells loaded with quin 2 were exposed compound 48/80 in a Ca-free medium, a marked increase of quin 2 fluorescence was noticed, indicating that Ca2+ was released from intracellular Ca store. The binding of 45Ca was at its peak in the fractions where the highest activity of glucose-6-phosphatase, a marker enzyme for the endoplasmic reticulum, when organelles of mast cells were fractionated. This may indicate that intracellular Ca store is endoplasmic reticulum. It has been shown that microfilaments, and microtubules play some important roles in histamine release from rat mast cells. When permeabilized mast cells were stimulated with Ca2+, a translocation of protein kinase C from cytosol to membrane fraction was observed. This leads to phosphorylation of vimentin, one of intermediate filaments. In membrane skeletons of rat mast cells, alpha- and beta-fodrin, ankyrin and actin were found by means of western blotting analysis. It was supposed that membrane skeleton may be useful as a barrier between the plasma membrane and the granule membrane.

Actin Cytoskeleton↗
PubMed1989

Spontaneous release of histamine from basophils and histamine-releasing factor in patients with atopic dermatitis and food hypersensitivity.

Patients with hypersensitivity to food documented by a double-blind, placebo-controlled oral food challenge have been reported to have a high rate of release of histamine from basophils in vitro. To determine whether patients with atopic dermatitis and food hypersensitivity had similar high rates of spontaneous histamine release in vitro, whether dietary elimination of relevant food antigens affected this release, and whether a cytokine, histamine-releasing factor, could account for it, we evaluated 63 patients with atopic dermatitis and food hypersensitivity (38 of whom had eliminated the offending foods from their diets), 20 patients with atopic dermatitis without food hypersensitivity, and 18 normal volunteers. Patients with atopic dermatitis and food hypersensitivity were found to have higher rates of spontaneous release of histamine from basophils than controls (mean +/- SE, 35.1 +/- 3.9 percent vs. 2.3 +/- 0.2 percent; P less than 0.001). Those who had eliminated the offending food allergen from the diet for an extended period had a significantly lower rate of histamine release (3.7 +/- 0.5 percent; P less than 0.001). In patients with atopic dermatitis without food hypersensitivity, the rate (1.8 +/- 0.2 percent) did not differ from that in normal controls. Mononuclear cells from persons with food allergies spontaneously produced a histamine-releasing factor in vitro that provoked the release of histamine from the basophils of other food-sensitive persons, but not from those of normal controls. Patients who adhered to a restricted diet had a decline in the rate of spontaneous generation of the factor by their mononuclear cells. The histamine-releasing factor was found to activate basophils through surface-bound IgE. We conclude that in patients with food hypersensitivity, exposure to the relevant antigens produces a cytokine (histamine-releasing factor) that interacts with IgE bound to the surface of basophils, causing them to release histamine.

Adolescent↗
PubMed1990

Carbohydrates inhibit the potentiating effect of bacteria, endotoxin and virus on basophil histamine release.

Histamine release caused by calcium ionophore A23187 and anti-IgE was examined in leukocyte suspensions from 8 healthy individuals. Staphylococcus aureus, lipopolysaccharide (LPS) from Salmonella typhimurium and influenza A virus were found to enhance the histamine release but did not release histamine per se. The potentiation of mediator release depends on a non-transient signal since the potentiating effect was also obtained by preincubation of the cells with LPS followed by wash-out and stimulation of the cells with anti-IgE. The potentiation was abolished or reduced by galactose, N-acetyl-glucosamine, alpha-methyl-D-glucoside, alpha-methyl-D-mannoside, N-acetylneuraminic acid and lactose, but not by glucose. These findings indicate that the enhancement of mediator release by bacteria, endotoxin, and virus depends on a sugar-mediated reaction.

Basophils↗
PubMedDate not supplied

Comparative study of the adverse effects of various radiographic contrast media, including ioversol, a new low-osmolarity medium. I. Histamine release.

Histamine release induced by some radiographic contrast media (RCM) such as iohexol, iopamidol and meglumine sodium amidotrizoate (MSA) was studied in comparison with ioversol, a new low-osmolarity contrast medium. Although all of the RCM caused a dose-related histamine release from rat peritoneal mast cells, that induced by ioversol was the least. MSA induced more remarkable histamine release than did sodium chloride at each of the corresponding osmolarities, except under hypoosmolar conditions. Moreover, in guinea pig lung perfusion, RCM, especially ioversol, iohexal and iopamidol, induced only a weak histamine release in both non-sensitized and sensitized animals. However, when MSA was perfused in sensitized animals, a large amount of histamine was detected in the lung effluents. These results suggest that nonionic RCM, including ioversol, can be used more safely than MSA for diagnostic examination.

Animals↗
PubMed1986

Regulation by serine esterase of histamine release from human leukocytes--I. Direct release of histamine by the serine esterase inhibitors diisopropyl fluorophosphate (DFP) and soman (GD).

The serine esterase inhibitor diisopropyl fluorophosphate (DFP) had been reported previously to inhibit IgE-dependent histamine release. Recently, it has been demonstrated that lower concentrations of DFP enhance IgE-dependent histamine release and inhibit desensitization. This manuscript describes the abilities of several esterase inhibitors to cause release of histamine from human leukocytes (basophils), by a process that is IgE-independent. This esterase inhibitor-induced histamine release appears to be by a non-cytotoxic mechanism that requires calcium and is temperature dependent. These histamine release processes occurred over a longer period of time than IgE-dependent release. Direct release of histamine by these small molecular weight inhibitors and inhibition of desensitization both suggest that one or more serine esterases are involved in the regulation of histamine release from human basophils.

Edetic Acid↗
PubMed1991

Aspects of the regulation of gastric histamine release.

Histamine is found in large amounts in the gastric mucosa and plays an essential role in the regulation of acid secretion. It is thought to stimulate acid secretion directly after being released by the other two major secretagogues (gastrin and acetylcholine) (the mediator hypothesis) or to potentiate the action of the other two secretagogues (the interaction hypothesis). Recent studies with isolated, vascularly perfused rat stomach have shown that gastrin in physiologic concentrations elicits a release of histamine sufficient to explain its acid-stimulatory effect. Vagal nerve stimulation, on the other hand, only gives a faint histamine release, indicating that the vagal acid stimulation is mainly mediated by a direct stimulation of the parietal cell. Furthermore, the gastrin-stimulated histamine release seems to be mediated by a calcium-dependent mechanism. Somatostatin inhibits gastrin-stimulated histamine release via a paracrine mechanism, and a prostaglandin E1 analogue (misoprostol) has been shown to be a potent inhibitor of base-line and gastrin-stimulated histamine release. These studies show that the modulation of histamine release may be a central regulatory mechanism of gastric acid secretion. Although these studies have been done in rats, there are indications that these results are of a general nature nd valid for other species as well.

Animals↗
PubMed1995

Effects of PBMC-derived histamine-releasing factors on histamine release from human skin and lung mast cells.

BACKGROUND: A field of study which has attracted much recent interest is the ability of mononuclear cells and neutrophils to interact with histamine releasing cells by production of specific histamine releasing factors (HRFs). However, almost all of these studies have been performed on basophils rather than human mast cells. OBJECTIVE: We have investigated the effects of lyophilized fractions of HRF preparations on histamine release from human skin and lung mast cells. METHODS: Lyophilized fractions of HRF preparations include crude supernatant from mononuclear cell/platelet (crude), void peak from anion exchange chromatography column (void), second peak from anion exchange chromatography (peak 2), neutrophil-activating peptide-2 (NAP-2), which was purified from void peak at molecular weight of 8-12 kDa, and monocyte chemotactic-activating factor (MCAF). Mast cells were enzymatically dispersed. RESULTS: Crude (24.2 micrograms/mL-2.42 mg/mL), void (5.4 micrograms/mL-0.54 mg/mL), peak 2 (3.5 micrograms/mL-0.35 mg/mL), and NAP-2 (1-20 micrograms/mL) failed to release histamine from lung mast cells. In skin mast cells, only higher concentrations of crude and void caused minimal release of histamine. MCAF up to micromolar concentrations failed to have an effect on mast cells from either source. However, these HRFs induced histamine release from human basophils. We also explored whether HRFs and stem cell factor could act as either priming agents for each other or for anti-IgE. The response of skin mast cells to all these preparations was not enhanced by preincubation in stem cell factor at 1 ng/mL, nor did the HRFs and MCAF enhance the response of skin mast cells to anti-IgE. CONCLUSION: These results suggest that these HRFs have no significant effect on dispersed human cutaneous and lung mast cells.

Basophils↗
PubMed1996

Modulation of pentagastrin-induced histamine release by histamine H3 receptors in the dog.

BACKGROUND: The histamine H3 receptor has been shown to inhibit pentagastrin-induced gastric acid secretion in dogs. Since pentagastrin releases histamine in dogs, we have now assessed whether the effects of H3-receptor ligands may be indirectly mediated by changes in gastric histamine release. METHODS: Pentagastrin infusions (1 or 6 micrograms/kg/h), alone or together with the H3-receptor agonist (R) alpha-methylhistamine (1.2 mumol/kg/h) or the antagonist thioperamide (0.1 mumol/kg/h), were performed in dogs. One group (anaesthetized) was used for enzyme immunoassays of plasma histamine and, when required. (R) alpha-methylhistamine in the gastrosplenic vein, and another group (non-anaesthetized) for measurement of gastric acid secretion. RESULTS: Histamine levels were increased five- and eight-fold after 1 and 6 micrograms/kg/h pentagastrin, respectively, whereas acid output was nearly maximal at the lower dosage. (R) alpha-methylhistamine, at a plasma concentration of 0.15 microM, inhibited histamine release by 78% (P < 0.007) and 37% (not significant) and the total acid output by 44% (P < 0.05) and 19% (not significant) after infusion of 1 and 6 micrograms/kg/h pentagastrin, respectively. Thioperamide, together with pentagastrin in low dose, significantly increased histamine release by 212% (P < 0.05), whereas acid output increased by 34% (not significant). CONCLUSIONS: The histamine H3 receptor mediates a negative feedback control of pentagastrin-induced release of gastric histamine. It is tonically activated by endogenous histamine after pentagastrin in low dosage. The control of acid secretion by the H3 receptor seems to involve modulation of endogenous histamine release, possibly by means of enterochromaffin-like cells.

Animals↗
PubMed1985

Comparison of histamine release in human skin mast cells induced by morphine, fentanyl, and oxymorphone.

Human leukocyte and skin mast cell preparations were incubated with morphine sulfate in concentrations ranging from 1.5 X 10(-5) M to 4.5 X 10(-3) M. Skin mast cells also were incubated with oxymorphone and fentanyl in the same concentrations. Human leukocytes did not release histamine in response to any concentration of morphine. In skin mast cells, histamine release by morphine first was detected at 1.5 X 10(-4) M. Histamine release further increased at 5.0 X 10(-4) M with no incremental increase at higher concentrations. Oxymorphone and fentanyl failed to release histamine at any concentration. Histamine release by morphine required calcium but was not influenced by changes in the 1-4 mM range. Skin mast cell preparations were pretreated for 30 min in naloxone 5 X 10(-4) M and then morphine 5 X 10(-4) M was added for 30 min without removing naloxone. Naloxone neither released histamine nor inhibited morphine-induced histamine release. The release of histamine by morphine but not equimolar concentrations of fentanyl and oxymorphone indicates that histamine release by narcotics is not a nonspecific effect of high drug concentration. The failure of naloxone to inhibit morphine-induced histamine release suggests that histamine release by morphine is not dependent on opiate receptor binding or activation. These results indicate that this human mast cell preparation will be useful in further understanding the mechanism of histamine release induced by morphine and other agents.

Cell Membrane↗
PubMed2003

Homogeneous time resolved fluorescence assay to measure histamine release.

Histamine is a biogenic amine synthesized by the enzymatic decarboxylation of histidine. Implication of histamine in allergy is well described but histamine is also found in some specific neurones, functions as a neurotransmitter and regulates sleep/wake cycles, hormonal secretion, cardiovascular control and thermo-regulation. We have developed a TR-FRET histamine assay, based on the competition between sample histamine and allophycocyanine (XL665) labelled histamine for binding to a Europium cryptate (EuK) labelled antibody. As histamine is a small monoamine molecule, high affinity antibodies have been raised against carrier protein conjugated histamine. Therefore, sample histamine needs to be derivatized in the same way as the conjugated histamine, so that the antibody will have a similar affinity for both molecules. This acylation step is performed directly in wells and does not need to be done in separate vials, making handling easier for large numbers of samples. The incubation takes place at room temperature for 3 hours. The assay covers a measurement range of 1.56 to 400 nM and shows an analytical sensitivity of 1.3nM. We have shown that miniaturization of sample and reagents volumes down to 20 micro l does not alter these performances. This histamine release assay provides a particularly well adapted procedure for HTS and secondary screening compared to current heterogeneous methods.

Basophils↗
PubMed1996

Histamine release in intact human skin by monocyte chemoattractant factor-1, RANTES, macrophage inflammatory protein-1 alpha, stem cell factor, anti-IgE, and codeine as determined by an ex vivo skin microdialysis technique.

BACKGROUND: The chemokines monocyte chemoattractant factor-1, RANTES, and macrophage inflammatory protein-1 alpha release histamine from human basophils, as well as rat and mouse mast cells. The purpose of this investigation was to determine whether these chemokines release histamine from human skin mast cells in situ. METHODS: A microdialysis technique was used to measure histamine release in skin. First, the model was validated by using anti-IgE, codeine, and stem cell factor (SCF); then the histamine-releasing effects of the chemokines were investigated. A total of 47 skin specimens from 41 donors were investigated. Hollow microdialysis fibers were inserted intradermally, and each fiber was slowly perfused (3 microliters/min). Anti-IgE, codeine, SCF, or chemokines were injected intradermally above individual fibers, and dialysate was collected at 2-minute intervals for 20 minutes. Each series of investigations comprised five to eight single experiments. RESULTS: Anti-IgE (4 to 4000 U/ml), codeine (0.001 to 1 mg/ml), and SCF (5.4 x (10(-11) to 10(-8) mol/L)) released histamine in a dose-dependent manner; maximum histamine release was 97.4, 116.3, and 9.5 pmol/20 min, respectively. Monocyte chemoattractant factor-1, RANTES, and macrophage inflammatory protein-1 alpha in concentrations of 10(-10) to 10(-6) mol/L did not release histamine; histamine release by 10(-6) mol/L chemokine was less than 0.2 pmol/20 min. None of the chemokines modulated anti-IgE-induced histamine release. In contrast, SCF significantly potentiated anti-IgE-induced histamine release by 33%. All chemokines, but not SCF, released histamine from human basophils. CONCLUSION: We conclude that the chemokines monocyte chemoattractant factor-1, RANTES, and macrophage inflammatory protein-1 alpha do not release histamine from human skin mast cells.

Aged↗