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PubMed1977

Automated histamine analysis for in vitro allergy testing. II. Correlation of skin test results with in vitro whole blood histamine release in 82 patients.

The recently developed sensitive, automated histamine assay system was applied for in vitro allergy testing. The simplified method for histamine release from whole heparinized blood was used. Aliquots of blood and allergen were incubated for one hour at 37 degrees C, and each supernatant was then analyzed for histamine release. Nine common pollen and environmental allergens were used at three 10-fold dilutions for in vitro testing with the use of 20 ml of blood. Intradermal skin tests were correlated with the whole blood histamine release in 82 patients who had received no immunotherapy. A scoring system for the histamine results was developed to take into consideration the results with multiple allergen concentrations. When the skin test was strongly positive (greater than or equal to 3 + at 100 protein nitrogen units [PNU]/ml), the whole blood histamine release was positive in 89% of the tests. In contrast, when the skin test was negative ( less than 1 + at 100 PNU/ml), the histamine release was also negative in 99.8% of the cases. When the skin test was 1 +, the histamine release from whole blood was positive in 6% of the tests; and when the skin test was 2+, the whole blood results were positive in 32%. The accuracy, precision, and sensitivity of the automated histamine assay allow its application for the clinical study of allergic patients.

Allergens↗
PubMed1979

Early effects of corticosteroids on basophils, leukocyte histamine, and tissue histamine.

The comparative effect in 11 atopic subjects of a single intravenous injection of methylprednisolone on sequential studies of blood eosinophils, basophils, leukocyte sensitivity to antigen for histamine release, leukocyte histamine content, and skin histamine was examined. No significant changes occurred in any parameter after placebo treatment. In contrast, 4 hr after intravenous treatment with steroid there were significant decreases in mean eosinophil counts (-95%), basophil counts (-72%), and histamine content of 1 X 10(7) leukocyte samples (-62%). Temporal changes in the latter paralleled alterations in circulating basophil levels. No significant changes occured in the antigen histamine release sensitivity, or the total skin histamine. Studies over a longer period after steroids in 4 subjects showed eosinophil and basophil levels at a nadir at 8 hr, remaining suppressed for 24 hr, and returned to pretreatment levels by 72 hr. Results suggest that corticosteroids induce a prominent decrease in leukocyte histamine due to a depletion of basophils without a decrease in histamine content per basophil, and that skin tissue histamine stores remain unchanged by such treatment.

Basophils↗
PubMed1990

Regulation of histamine H1 receptor-mediated phosphoinositide hydrolysis by histamine and phorbol esters in DDT1 MF-2 cells.

The regulation of histamine-stimulated phosphoinositide turnover by histamine and phorbol esters was examined in intact DDT1 MF-2 cells grown in suspension culture. Histamine increased the incorporation of 32P into phosphatidylinositol (PI) in these cells, and this stimulation was inhibited by the H1 antagonist diphenhydramine but not by the H2 antagonist cimetidine. Pretreatment of cells with histamine or with phorbol 12-myristate 13-acetate (PMA) or other activators of protein kinase C induced a marked decrease in the subsequent stimulation by histamine. PMA, but not histamine, also decreased the ability of epinephrine to stimulate PI labelling through alpha 1-adrenoceptors. Thus, histamine appears to induce homologous desensitization of histamine H1 receptor-mediated PI turnover, whereas direct activation of protein kinase C in the absence of receptor occupancy by agonist induces nonspecific heterologous desensitization of both histamine H1- and alpha 1-adrenoceptor-mediated responses.

Animals↗
PubMed1999

Histamine and histamine-receptor antagonists modify gene expression and biosynthesis of interferon gamma in peripheral human blood mononuclear cells and in CD19-depleted cell subsets.

The effect of histamine and histamine antagonists was examined on gene expression and biosynthesis of bacterial endotoxin (LPS) induced interferon gamma (IFNgamma) both in human peripheral mononuclear cells (PMBC) and in T-cell enriched fractions. We found, that histamine inhibited the LPS induced transcription of IFNgamma gene and biosynthesis of IFNgamma protein in PMBC and also in CD19-depleted cell populations. The inhibitory effect of histamine could be reversed by the H2 histamine receptor (HR2) antagonists cimetidine and ranitidine both in PMBC and in CD19-depleted cells, but not with triprolidine, an H1 receptor antagonist, suggesting that the inhibition of IFNgamma production is mediated through H2 receptors in these cell populations. In contrast to the inhibitory effect of histamine, cimetidine alone (in the absence of exogenous histamine) strongly stimulated both the IFNgamma mRNA and protein production, whereas this effect was hardly seen by and other H2 receptor blocker, ranitidine. This superinduction of IFNgamma gene by cimetidine disappeared if the CD19+ cells are removed from PMBC. These results suggest, that inhibition of IFNgamma gene expression by histamine is a direct effect of histamine on H2 receptor of T lymphocytes; however, the superinduction of IFNgamma by cimetidine requires the presence of other (probably primarily B) cell subsets.

Antigens, CD19↗
PubMed1999

Diesel exhaust particulates upregulate histamine receptor mRNA and increase histamine-induced IL-8 and GM-CSF production in nasal epithelial cells and endothelial cells.

BACKGROUND: Histamine is the most important chemical mediator in the pathogenesis of nasal allergy. Diesel exhaust particulates (DEPs) are common air pollutants from diesel engine-powered car exhaust and cause chronic airway diseases. Recently we observed that the nasal reactivity to histamine was enhanced in diesel exhaust-exposed guinea-pigs. It was also revealed that epithelial cells and endothelial cells in the airway produce certain cytokines in response to histamine. OBJECTIVE: We examined the effects of DEP extract on the expression of histamine H1 receptor (H1R) mRNA in human nasal epithelial cells (HNECs) and human mucosal microvascular endothelial cells (HMMECs), and on the production of IL-8 and GM-CSF induced by histamine. METHODS: HNECs and HMMECs were isolated from human nasal mucosa specimens. HNEC and HMMEC monolayers were cultured in the presence or absence of DEP extract. The change in the expression of H1R mRNA was then evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR) and the Southern blot analysis. To investigate the effects of DEP extract on the histamine-induced cytokine production, HNEC and HMMEC monolayers were cultured in the presence or absence of DEP extract for 3-24 h. After three washes with PBS, they were then incubated with 10(-6) mol/L histamine for 24 h. The amounts of IL-8 and GM-CSF in the culture media were measured by enzyme-linked immunoabsorbent assay. RESULTS: DEP extract increased the expression of H1R mRNA in both HNECs and HMMECs. The amount of IL-8 and GM-CSF, induced by histamine, was significantly higher in DEP extract pretreated HNECs and HMMECs than nontreated HNECs and HMMECs. CONCLUSION: These results strongly suggest that DEP accelerates the inflammatory change by not only directly upregulating H1R expression but also increasing histamine-induced IL-8 and GM-CSF production.

Cell Survival↗
PubMed1991

Histamine suppresses gene expression and synthesis of tumor necrosis factor alpha via histamine H2 receptors.

Histamine and tumor necrosis factor alpha (TNF-alpha) can each contribute to the pathogenesis of allergic reactions and chronic inflammatory diseases. We now report the effect of histamine on gene expression and total cellular synthesis of TNF-alpha. Lipopolysaccharide (LPS)-induced synthesis of TNF-alpha in peripheral blood mononuclear cells (PBMC) from 18 healthy donors was suppressed by histamine concentrations from 10(-6) to 10(-4) M, levels comparable with those measured in tissues after mast cell degranulation. Histamine (10(-5) M) markedly suppressed LPS-induced synthesis of TNF-alpha in both unfractionated PBMC (83% inhibition, p less than 0.001) and monocytes purified by positive selection of LeuM3+ cells (62% inhibition, p less than 0.05). The suppressive effect of histamine on TNF-alpha synthesis did not require the presence of T cells. The histamine-mediated decrease in TNF-alpha synthesis was not affected by indomethacin, nor by diphenhydramine, an H1 receptor antagonist, but was reversed by cimetidine or ranitidine, H2 receptor antagonists, in a dose-dependent manner. Suppression of TNF-alpha synthesis by histamine is likely to be a transcriptional event, since histamine (10(-5) M) reduced TNF-alpha mRNA levels fourfold. These results suggest that histamine release from mast cells may paradoxically limit the extent of inflammatory and immune reactions by suppressing local cytokine synthesis in H2 receptor-bearing cells.

Cells, Cultured↗
PubMed1977

A simplified method for measuring basophil histamine release and blocking antibodies in hay fever patients. Basophil histamine content and cell preservation.

A simplified method for measuring basophil histamine release in grass pollen hay fever patients has been developed. Leukocytes were challenged in vitro with extracts of Phleum pratense (timothy) and the release of histamine was determined indirectly as the residual histamine in the cell sediment. Several steps to purify histamine thus became superfluous and histamine was directly conjugated with o-phthaldialdehyde to form a fluorophore. The simplified method showed a basophil histamine content which was in accordance with results obtained by more specific methods. No difference in basophil histamine content was found between normal and allergic persons. For the histamine liberation assay blood could be adequately preserved for transport for 48 h at room temperature by adding cell culture medium. Basophil histamine release technique allows evaluation of cell sensitivity for determination of the degree of allergy as well as the level of blocking antibodies.

Adult↗
PubMedDate not supplied

Co-localization of histamine and dopamine-beta-hydroxylase in sympathetic ganglion and release of histamine from cardiac sympathetic terminals of guinea-pig.

1. The aim of this study was to investigate the co-localization of histamine and dopamine-beta-hydroxylase in the superior cervical ganglion of guinea-pig and release of histamine from cardiac sympathetic terminals in guinea-pig isolated atrium. 2. Histidine decarboxylase (a histamine-synthesizing enzyme) mRNA signals were detected in the neurones of superior cervical ganglion of guinea-pig by in situ hybridization. The results of double-labelled immunofluorescence further confirmed the co-localization of histamine and dopamine-beta-hydroxylase in the large principle neurons and small intensely fluorescent cells in the superior cervical ganglion. The immunoreactivities of both histamine and dopamine-beta-hydroxylase were significantly attenuated after 6-hydroxydopamine-induced lesion of sympathetic nerves. 3. The refractory electrical field stimulation caused the release of histamine from cardiac sympathetic terminals of guinea-pig isolated atria (112.14 +/- 40.34 ng x ml(-1)), which was significantly attenuated to 35 +/- 15.57 ng x ml(-1) by reserpine pretreatment. Following administering compound 48/80, a mast cell degranulator, electrical field stimulation induced a dramatic increase of endogenous histamine release from isolated atria (303.57 +/-72.93 ng x ml(-1)). When compound 48/80 was added to the reserpine-treated atria, the release of histamine induced by field stimulation was decreased to 207.14 +/- 76.39 ng x ml(-1). 4 These results provide novel evidence that histamine co-exists with noradrenaline in sympathetic nerves and might act as a neurotransmitter to modulate sympathetic neurotransmission.

Animals↗
PubMed1988

Biphasic effects of intra-accumbens histamine administration on spontaneous motor activity in the rat; a role for central histamine receptors.

1. The effect of intra-accumbens injection of histamine and related compounds on the spontaneous motor activity of the rat has been investigated. 2. Microinjections of histamine (1-200 micrograms) induced dose-dependent, biphasic changes in rat activity consisting of an initial brief hypoactivity response followed by a marked hyperactivity phase. The histamine metabolite, n-tele-methylhistamine was without effect. 3. Pretreatment with the H1-receptor antagonist mepyramine (10 micrograms) blocked the hypoactivity response and markedly attenuated histamine-induced hyperactivity. In contrast, pretreatment with the H2-receptor antagonist SKF93479 had no effect on histamine-induced behaviour. 4. Microinjection of the H1-receptor agonist 2-thiazolylethylamine induced a marked hyperactivity response, but unlike the response to histamine, there was no initial hypoactivity. The H2-receptor agonist dimaprit had no apparent behavioural effects following intra-accumbens injection. 5. Intra-accumbens injection of the non-selective histamine agonists n alpha-methylhistamine or n alpha, n alpha-dimethylhistamine induced both marked hypoactivity and hyperactivity responses which were comparable with the effects of histamine. 6. The present results demonstrate a histamine, H1-receptor-mediated arousal in the nucleus accumbens which follows transitory hypoactivity, possibly due to activation of presynaptic H3-receptors.

Animals↗
PubMed1996

Nitrogen dioxide exposure increases airway contractile response to histamine by decreasing histamine N-methyltransferase activity in guinea pigs.

To determine the mechanism responsible for nitrogen dioxide (NO2)-induced airway hyperresponsiveness, we examined the effects of NO2 exposure on the contractile response to histamine and the level of histamine N-methyltransferase (HMT) activity, a histamine-degrading enzyme, in guinea pig trachea in vitro. Guinea pigs were divided into seven groups. Each group received continuous NO2 exposure (2.0 ppm) for either 2, 6, 12, 24, 48, or 96 h. The remaining group did not receive NO2 exposure (control). HMT activity in trachea was decreased from the control value of 70.3 +/- 7.7 pmol/min/mg protein to 34.6 +/- 6.7 pmol/min/mg protein by 12 h exposures of NO2. However, 24 and 48 h exposures of NO2 did not significantly alter HMT activity. In contrast, HMT activity exceeded the control value by 96 h exposures of NO2 (85.5 +/- 5.1 pmol/min/mg protein). Twelve hour exposures of NO2 shifted the concentration-response curves to histamine to lower concentrations and significantly reduced the median effective concentration (EC50) of histamine (log M) from the control value of -5.16 +/- 0.09 to -6.15 +/- 0.14 (P < 0.01). In contrast, the EC50 concentration of histamine (log M) increased from the control value of -5.20 +/- 0.10 to -4.90 +/- 0.11 by 96 h exposures of NO2 (P < 0.05). However, NO2 exposure did not alter the contractile response to acetylcholine. Morphologically, tracheal epithelial cells had vacuoles after 12 h exposures of NO2, but denudation of the epithelium did not occur during this experiment. In situ hybridization for HMT mRNA demonstrated that the level of HMT mRNA increased dominantly in tracheal epithelial cells after 96 h exposures of NO2. The present results indicated that the decrease in the level of HMT activity in the trachea was closely associated with the increase in the airway contractile response to histamine, suggesting that NO2-induced transient airway hyperresponsiveness to histamine is due to the decreased capacity of histamine catabolism in airway.

Animals↗
PubMed1989

[Studies on the degranulation and histamine release of purified rat peritoneal mast cells. The inhibitory effect of histamine and other chemicals].

We know that the mast cell or basophil degranulation and the release of chemical mediators such as histamine may play an important role in inducing immediate type allergic reactions. In this experiment, employing purified rat peritoneal mast cells (RPMC) the degranulation pattern of RPMC and percent release of histamine from RPMC by pharmacologic (compound 48/80, kallikrein or peptidoglycan) or allergic (IgE-anti IgE complex) stimuli were examined. The inhibitory effects of catecholamine (isoproterenol), an adenylate cyclase stimulator, methylxanthine (IBMX: 3-isobutyl-1-methyl-xanthine), a phosphodiesterase inhibitor and chemical mediators (histamine, serotonin, bradykinin) on compound 48/80-induced RPMC degranulation and also those of catecholamine, methylxanthine and chemical mediators on IgE-anti IgE complex-induced histamine release from RPMC were tested. Compound 48/80-induced RPMC degranulation was remarkably inhibited not only by treatment with isoproterenol and IBMX, but also by treatment with histamine. It was not, however, inhibited by serotonin or bradykinin. The inhibitory effect of histamine on compound 48/80-induced RPMC degranulation was blocked by pretreatment with H2-antagonist (cimetidine), but not by H1-antagonist (diphenhydramine). The cyclic adenosine 3',5'-monophosphate (cAMP) content of RPMC was significantly increased by pretreatment with histamine as well as isoproterenol and IBMX. These facts suggest that cAMP acts as a regulator or modulator of the RPMC degranulation and the histamine release from mast cells and that the inhibitory effect induced by histamine may be related to the H2-receptor existing on the surface of mast cells.

Animals↗
PubMed2004

To evaluate and compare the effects of first generation anti-histamine (chlorpheniramine maleate) and second generation anti-histamine (loratadine) on isolated trachea of rabbit.

OBJECTIVE: The incidence of respiratory allergy has increased gradually over the past several years and current estimates suggest that allergic rhinitis affects approximately 20% of the population. Large scales population surveys indicate that up to 38% of patients with rhinitis have asthma. The allergic response in the airways is an important pathogensis to cause bronchoconstriction owing to increased responsiveness of tracheo bronchial tree to various stimuli and also causes the release of histamine and other chemical mediators from mast cells. Histamine has been shown to be an important mediator of an allergic reaction in both the upper and lower respiratory airways. Chlorpheniramine maleate is a stable, most potent, sedative first generation anti-histamine and is effective in the treatment of allergic disorders. Loratadine is a highly potent, non-sedating, long acting tricyclic, second generation anti-histamine. It is indicated in allergic rhinits, chronic idiopathic urticaria and allergic bronchial asthma. The purpose of study was to evaluate the antagonistic effects of chlorpheniramine maleate and loratadine on histamine induced contractions in isolated trachea of rabbit and also to compare the effects of first generation anti-histamine (chlorpheniramine maleate and second generation anti-histamine loratadine). METHODS: In this study twenty-four experiments were performed on isolated trachea of rabbit, in the presence of selected standard concentration of histamine dihydrochloride, antagonistic effects of various concentrations of chlorpheniramine maleate (10-18 to 10(-3) gm/ml) and loratadine from concentrations 10(-18) to 10(-3) gm/ml were recorded by Polygraph Model 7B in terms of rate and amplitude. RESULTS: Chlorpheniramine maleate showed non-significant antagonistic effect from concentrations 10(-18) to 10(-3) gm/ml in case of rate and 10(-18) to 10(-8) gm/ml in case of amplitude. Significant response showed from concentrations 10(-8) to 10(-3) gm/ml in case of rate (P<0.001) and 10(-7) to 10(-3) gm/ml in case of amplitude (P<0.001) while, loratadine showed non-significant response from concentrations 10(-18) to 10(-12) gm/ml in case of rate and from concentration 10(-18) to 10(-14) gm/ml in case of amplitude. Significant response observed from concentrations 10(-11) to 10(-3) gm/ml in case of rate and 10(-13) to 10(-3) gm/ml in case of amplitude. CONCLUSION: It was concluded that chlorpheniramine maleate antagonized the histamine induced contractions 80.65% at concentration 10(-3) gm/ml in case of amplitude and 11.35% at concentration 10(-3) gm/ml in case of rate and loratadine 76.82% in case of amplitude and 10.59% in case of rate.

Animals↗
PubMed2004

Histamine enhances cytotrophoblast invasion by inducing intracellular calcium transients through the histamine type-1 receptor.

Blastocyst implantation and placentation require molecular and cellular interactions between the uterine endometrium and blastocyst trophectoderm. Previous studies showed that histamine produced in the mouse uterine luminal epithelium interacts with trophoblast histamine type-2 receptors (H2) to initiate blastocyst implantation. However, it is unknown whether similar histamine activity is operative in humans. Using a human cell line (HTR-8/SVneo) derived from first-trimester cytotrophoblasts that expresses both histamine type-1 receptor (H1) and H2, we found that histamine promotes cytotrophoblast invasiveness specifically through activation of H1. Stimulation of H1 in human cytotrophoblasts by histamine induced intracellular Ca2+ (Ca(2+)i) transients by activating phospholipase C and the inositol trisphosphate pathway. The enhanced invasion induced by histamine was blocked by pretreatment with H1 antagonist or by chelation of Ca(2+)i. These findings suggest possible differences between rodents and humans in histamine signaling to the trophoblast.

Calcium↗
PubMed1982

Histamine receptors of the microvascular endothelium revealed in situ with a histamine-ferritin conjugate: characteristic high-affinity binding sites in venules.

Histamine covalently bound to glutaraldehyde-activated ferritin was prepared as either monomers or as small aggregates of approximately 0.05 to 0.15 micrometer Diam, suitable for electron microscopic detection of histamine cellular binding sites. The histamine-ferritin conjugates (MF) maintain the histamine capability to induce the opening of endothelial junctions in venules. To investigate the distribution of histamine receptors in the vascular endothelium, monomers or aggregates of MF were perfused in situ (mice), and various vascular beds, particularly that of the diaphragm, were fixed and processed for electron microscopy. The conjugate was preferentially bound on restricted areas of luminal endothelial cell plasmalemma especially in regions rich in filaments, and near the junctions between endothelial cells. The density of histamine binding sites was characteristically high in venules; it occurred to a much lesser extent in arterioles, veins, and muscular arteries whereas capillaries and aorta showed the lowest values. A similar distribution was obtained after perfusion of H1 or H2 receptor agonists coupled to ferritin (2-pyridylethylamine-ferritin [PF], or 4-methylhistamine-ferritin [MF], respectively). The binding specificity was assessed through control experiments with either native or activated ferritin or by competition with histamine. The findings suggest that histamine receptors are largely represented in the cell membrane of the vascular endothelium, particularly in venules. Experiments using specific H1 and H2 receptor agonists (PF and MF) and antagonists (mepyramine and cimetidine) indicate that the venular endothelium contains mainly H2 receptors.

Animals↗
PubMed1987

Binding of histamine-albumin conjugates to human lymphocytes: evidence for labelling of histamine H-1 but not H-2 receptors.

Histamine conjugated to human serum albumin (HSA) bound to a major proportion of human peripheral blood lymphocytes in a rosetting assay. In contrast, red cells coated with the control conjugates pentylamine-HSA and ethanolamine-HSA were unreactive. Amine conjugation by the carbodiimide method imposed a positive charge on the albumin molecule. However, the percentage histamine-HSA-binding lymphocytes was related to the amount of histamine coupled to the albumin molecule and not to differences in isoelectric point (pI) of the modified protein carriers. Four different histamine-albumin conjugates and one pentylamine-HSA conjugate inhibited lymphocyte binding of histamine-HSA, whereas ethanolamine-albumin, carbodiimide-reacted HSA and native albumin were not inhibitory. The histamine H-2 receptor antagonists cimetidine, ranitidine, metiamide, and burimamide lacked inhibitory effects. The histamine H-1 receptor antagonists clemastine, mepyramine, and diphenhydramine efficiently inhibited lymphocyte binding of the histamine-albumin conjugate with IC50 values of 0.2, 1, and 40 mM, respectively, indicating interactions with low affinity H-1 receptors.

Binding, Competitive↗
PubMed1978

Central cardiovascular actions of histamine in rats: involvement of histamine H2-receptors.

Centrally induced pressor effects, associated with tachycardia have previously been demonstrated after intraventricular (i.c.v.) injections of histamine. The selective histamine H2-receptor agonists dimaprit (1--500 microgram) and 4-methyl histamine (1--10 microgram), and the histamine H1-receptor agonist 2-methyl histamin (1--10 microgram) elicited rises in blood pressure and heart rate after i.c.v. administration in urethane-anaesthetised rats. Metiamide (400--800 microgram, i.c.v.) antagonised the cardiovascular responses induced by dimaprit and 4-methyl histamine, but not the responses induced by 2-methyl histamine. In contrast mepyramine (100 microgram, i.c.v.) failed to antagonise the dimaprit-induced effects. It is concluded that histamine H1 and H2-receptors are present in the central nervous system of rats. Selective stimulation of either H1- or H2-receptors can lead to pressor effects associated with tachycardia after i.c.v. administration of specific agonists in urethane-anaesthetised rats. These responses are selectively antagonised by the respective receptor antagonists.

Animals↗
PubMedDate not supplied

Autoregulation of histamine release via the histamine H3 receptor on mast cells in the rat skin.

The autoregulation of the histamine release via the histamine H3 receptor in the periphery was studied in vivo and in vitro. Antidromic electrical stimulation of the sciatic nerve caused a significant increase in histamine release in the subcutaneous perfusate in the rat hindpaw. (R)alpha-methylhistamine, a specific H3 receptor agonist, significantly and dose-dependently inhibited the increase in release of histamine by antidromic stimulation at intravenous doses of 0.25-2 mg/kg. Thioperamide (2 mg/kg, intraperitoneally), a specific H3 antagonist, prevented the inhibitory effect of (R)alpha-methylhistamine. Substance P perfusion (5-50 microM) also elicited a significant increase in histamine, and a significant inhibition by (R)alpha-methylhistamine and the antagonism of thioperamide were observed. (R)alpha-methylhistamine inhibited the histamine release by substance P from rat peritoneal mast cells in vitro, and thioperamide reduced the response to (R)alpha-methylhistamine. These data suggest that mast cells may have histamine H3 receptors, and that histamine probably modulates its own release through the H3 receptor in neurogenic inflammation.

Analysis of Variance↗
PubMed2006

Circadian variations of histamine binding to lymphocytes and neutrophils and skin reactivity to histamine in atopic and healthy subjects.

INTRODUCTION: Numerous pathophysiological conditions change during 24-hour periods. Histamine, the main mediator in allergic reactions, exerts a multiplicity of pathophysiological actions through binding to specific receptors on effector cells. Nocturnal exacerbation of symptoms occurs in many atopic diseases in which histamine is an important mediator. Nocturnal wheezing is a very common symptom of asthma. The aim of this study was to determine whether the binding of (fluorescein-labeled) histamine to cells participating in allergic-inflammatory processes (lymphocytes, neutrophils) and skin reactivity to histamine undergo circadian changes and to compare these phenomena in atopic asthmatic and healthy subjects. MATERIALS AND METHODS: Blood samples were collected at 8 am, 2 pm, 8 pm, 2 am, and 8 am the next day. Histamine skin-prick tests were performed at the same times. RESULTS: It was found that skin reactivity to histamine (wheal, erythema) in healthy subjects underwent significant circadian changes with acrophase at 8 am (wheal) or 8 pm (erythema), the lowest values being at night (2 am, p = 0.017), in contrast to atopics, in whom the highest reactivity was found at night (2 am, p = 0.002). Significant differences in the binding of fluorescein-labeled histamine between day (8 am-2 pm) and night (2 am) were observed for lymphocytes (p = 0.006) and neutrophils (p = 0.018). CONCLUSIONS: In the asthmatic group these changes were not significant. Circadian changes in both the binding of histamine by effector cells and skin reactivity to histamine were different in healthy and asthmatic subjects, and this may play a role in the pathomechanism, course, and chronopharmacotherapy of atopic diseases.

Adult↗