Regulation of histamine release from human basophil leucocytes: role of H1, H2 and H3 receptors

Tedeschi, A.; Lorini, M.; Arquati, M.; Miadonna, A.

doi:10.1111/j.1398-9995.1991.tb00634.x

Cited by 26 publications

(13 citation statements)

References 19 publications

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“…Activated basophils release stored histamine using a degranulation mechanism. Histamine affects many cells (for review see [42,43]) and even the basophils themselves by binding with the H2 receptors (H2R) [44][45][46] and by mediating the reregulation of further histamine release. This negative regulation mechanism on anti-IgE-activated basophils ( fig.…”

Section: Discussionmentioning

confidence: 99%

Sensitive Flow Cytometric Method to Test Basophil Activation Influenced by Homeopathic Histamine Dilutions

Lorenz¹,

Schneider

Stolz³

et al. 2003

Complement Med Res

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Objective: In an experimental setting, human basophil degranulation was triggered by anti-IgE to measure the effects from homeopathic solutions in an in-vitro cell system. A 3-color flow cytometric method with enhanced accuracy was established. As an example we looked at the influence of histamine on anti-IgE activation of basophils. Methods: Basophils were identified in the flow cytometer by their physical properties in the forward and side scatter light depiction and by gating on CD2^–, CD14^–, CD16^–, CD19^–, HLA-DR^– negative and CD123-positive cells. CD63 expression on the cell surface of the anti-IgE-activated basophils served as an activation marker. Results: With this method we were able to study basophil function of the 0.6–3.9% basophils out of the mononuclear blood cell fraction and to document their activation status upon anti-IgE activation. Optimal activation occurs at 0.6 µg/ml final anti-IgE concentration; not less than 10,000 basophils have to be counted per batch to reduce the variation of the measurement. The fixation method was able to stabilize activation for two days. After investigation and reduction of the source of measurement variability, an unequivocally inhibited basophil activation was documented in a partly optimized system with homeopathic dilutions of histamine (10^–22M, 10^–23M, 10^–24M, and 10^–25M histamine). Dilutions greater than 10^–20M histamine (Avogadro’s number 6.02 × 10²³) account for less than 1.36 molecules of histamine in the test sample, indicating a true homeopathic effect. Conclusions: This test system is adequate for studying the effects of highly diluted mediators on basophil activation by anti-IgE. The systematic application of this experimental arrangement is recommended to study the effects of homeopathic dilutions on basophils.

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Section: Discussionmentioning

confidence: 99%

Sensitive Flow Cytometric Method to Test Basophil Activation Influenced by Homeopathic Histamine Dilutions

Lorenz¹,

Schneider

Stolz³

et al. 2003

Complement Med Res

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“…Since total cellular histamine is low, the extent of such an early release would be limited, as shown in Table 2 by the absolute amount of released histamine lower at pre-treatment than at 21 days post-treatment, thus preventing the onset of hypersensitivity reactions after treatment. Additionally, any such early in vivo release of histamine may down-regulate further release through an autocrine mechanism involving H2 receptors [27]. …”

Section: Resultsmentioning

confidence: 99%

Changes in IgE- and Antigen-dependent histamine-release in peripheral blood of Schistosoma mansoni-infected Ugandan fishermen after treatment with praziquantel

et al. 2004

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Background: Parasite-specific IgE levels correlate with human resistance to reinfection with Schistosoma spp. after chemotherapy. Although the role of eosinophils in schistosomiasis has been the focus of a great deal of important research, the involvement of other Fcε receptor-bearing cells, such as mast cells and basophils, has not been investigated in relation to human immunity to schistosomes. Chemotherapy with praziquantel (PZQ) kills schistosomes living in an in vivo blood environment rich in IgE, eosinophils and basophils. This releases parasite Ags that have the potential to cross-link cell-bound IgE. However, systemic hypersensitivity reactions are not induced by treatment. Here, we describe the effects of schistosomiasis, and its treatment, on human basophil function by following changes in total cellular histamine and in vitro histamine-release induced by schistosome Ags or anti-IgE, in blood samples from infected Ugandan fishermen, who are continuously exposed to S. mansoni infection, before and 1-day and 21-days after PZQ treatment.

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“…Human basophils have been proven to have H2-recep tors, stimulation of which elevates the intracellular levels of cyclic 3',5'-adenosine monophosphate to inhibit anaphylactic histamine release (18). In addition, it has been reported that cimetidine enhances the release by a blockade of the receptor (19). Furthermore, in human lung mast cells, anaphylactic histamine release is also demonstrated to be blocked by stimulation of their H2 receptor (20).…”

Section: Histamine Levels In Rat Plasmasmentioning

confidence: 93%

Possible Participation of Histamine H3-Receptors in the Regulation of Anaphylactic Histamine Release from Isolated Rat Peritoneal Mast Cells

Kohno

Nakao

Ogawa

et al. 1994

Japanese Journal of Pharmacology

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ABSTRACT-Anaphylactic histamine release from isolated rat peritoneal mast cells was concentration dependently blocked by a 5-min treatment with exogenous histamine at 0.9 and 9 pM and enhanced by a 20 to 30-min treatment with thioperamide (H3-antagonist) at 3 pM with significance, but little affected by mepyramine (H,-antagonist) and cimetidine (H2-antagonist) at the cell concentration of 106 mast cells/ml. At a low concentration of mast cells (104 mast cells/ml), (R)-a-methylhistamine (a-MH), an H3-agonist, at 0.9-90 pM also inhibited the release in a concentration-dependent fashion. Thioperamide, but neither mepyramine nor cimetidine, significantly restored the decreased release by a-MH. However, the complete restoration by thioperamide could not be achieved because the drug itself slightly but concentration dependently inhibited anaphylactic histamine release. On the other hand, not only betahistine and dimaprit but also a-MH did not suppress histamine release from the mast cells induced by compound 48/80. In rat plasma, considerable levels of histamine were detected. From these results, it is strongly suggested that histamine H3-like receptors are largely responsible for the negative feedback regulation of the anaphylactic histamine release from rat peritoneal mast cells. In the early 1980s, a third receptor of histamine was identified, which regulates the synthesis and release of histamine in the histaminergic nerve ends in the rat brain, and this was designated as the H3-receptor (1).Since then, the development of specific and selective agonists and antagonists of histamine receptor subtypes has revealed that H3-receptors exist in other tissues in cluding the ileum (2), airway (3, 4) and blood vessels (5); this was concluded from the observations that the neural stimulation-induced twitch responses of these tissues are inhibited by modulation of ACh, neuropeptides and other neurotransmitter release by H3-receptor stimula tion, in a similar manner to that of the rat cerebral cortex. Thus, the majority of the investigations on H3-receptors were initially focused on the modulation of neurotrans mitter release and/or histamine synthesis in the presynap tic ends of the brain or other tissues. In addition, there have recently been a number of reports on the roles of the receptor in effector organs: H3-receptor stimulation relaxed rabbit middle cerebral artery preconstricted with K+ by acceleration of nitric oxide and prostacyclin forma tion from the endothelium (6, 7); an H3-antagonist aggra vated experimental allergic asthma in the guinea pig (8); an H3-agonist and H3-antagonist inhibited and enhanced, respectively, the histamine release from isolated gastric glands (9), and H3-receptor stimulation specifically down regulated histamine synthesis in isolated fundic mucosal cells (10) in rabbits; an H3-receptor agonist reduced gas trin-induced vascular histamine release in the isolated rat stomach (11).In the present study, we obtained evidence indicating that isolated rat peritoneal mast cells have surface H3 re...

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Regulation of histamine release from human basophil leucocytes: role of H₁, H₂ and H₃ receptors

Cited by 26 publications

References 19 publications

Sensitive Flow Cytometric Method to Test Basophil Activation Influenced by Homeopathic Histamine Dilutions

Sensitive Flow Cytometric Method to Test Basophil Activation Influenced by Homeopathic Histamine Dilutions

Changes in IgE- and Antigen-dependent histamine-release in peripheral blood of Schistosoma mansoni-infected Ugandan fishermen after treatment with praziquantel

Possible Participation of Histamine H3-Receptors in the Regulation of Anaphylactic Histamine Release from Isolated Rat Peritoneal Mast Cells

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