Role of histamine in natural killer cell-dependent protection against herpes simplex virus type 2 infection in mice

Hellstrand, Kristoffer; Asea, Alexzander; Hermodsson, Svante

doi:10.1128/cdli.2.3.277-280.1995

Cited by 6 publications

(5 citation statements)

References 20 publications

(22 reference statements)

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“…Thus, histamine-treated mice are partially protected against HSV-2-induced encephalitis whereas ranitidine markedly reduces survival time. Histamine is synergistically protective in this model when administered together with IL-2, and the effects of histamine in viral encephalitis depend on an intact population of NK cells in vivo [13].…”

Section: Introductionmentioning

confidence: 80%

“…Combined treatment with histamine and IL-2 has been shown to effectively protect mice against B16 melanoma metastasis [12] as well as HSV-2-induced encephalitis [13]. Furthermore, histamine and IL-2 synergistically augment the cytotoxicity of human NK-cells in vitro [4], but the effects of combined treatment with histamine and IL-2 on NK-cell cytotoxicity in vivo is not known.…”

Section: Augmentation Of Nk-cell Dependent Clearance Of Yac-1 Cells Bmentioning

confidence: 99%

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Histaminergic Regulation of Natural Killer Cell‐Mediated Clearance of Tumour Cells in Mice

1996

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Treatment of Swiss albino mice with histamine enhanced the clearance of natural killer (NK)-cell sensitive YAC-1 lymphoma and B16/F10 melanoma cells from lung tissue in vivo, but did not affect the elimination of NK-cell-insensitive P815 mastocytoma cells. The effect of histamine was apparently mediated by H2-type histamine receptors (H2R) since it was blocked by ranitidine, and H2R antagonist. Histamine did not affect clearance of tumour cells in animals depleted of NK cells in vivo by treatment with antibodies to asialo-GM1 or NK1.1. The effect of histamine was time-dependent: pretreatment with histamine for 3 h significantly augmented the clearance of YAC-1 cells, whereas, pretreatment with histamine for 5 min was ineffective. Histamine potentiated the anti-tumour properties of NK-cell activators such as interleukin-2 (IL-2) or interferon-alpha (IFN-alpha) in vivo. None of these lymphokines significantly affected the clearance of YAC-1 cells unless animals were concomitantly treated with histamine. Treatment with ranitidine alone reduced the in vivo clearance of YAC-1 cells from lungs but did not affect the clearance of NK-cell-insensitive P815 cells. Effects of ranitidine on NK-cell function in vivo were not shared by a chemical control to ranitidine, AH20239AA, thus indicating that the inhibition of NK-cells results from H2R antagonism rather than non-specific toxicity. It is concluded that histaminergic mechanisms may be involved in the regulation of NK cell function in vivo.

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Section: Introductionmentioning

confidence: 80%

Section: Augmentation Of Nk-cell Dependent Clearance Of Yac-1 Cells Bmentioning

confidence: 99%

Histaminergic Regulation of Natural Killer Cell‐Mediated Clearance of Tumour Cells in Mice

1996

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“…Before surgery, mice were allocated either to continuous infusion of angiotensin II (AngII, diluted in heparinized isotonic glucose solution (100 IU mL −1 ), infusion rate 60 ng kg −1 min −1 ) [ 36 ] to induce hypertension or to infusion with the histamine H 2 -receptor antagonist ranitidine (27.8 µg kg −1 min −1 ) [ 24 ] in combination with AngII (ranitidine+AngII). During anesthesia (100 mg kg −1 ketamine and 10 mg kg −1 xylazine I.P.…”

Section: Methodsmentioning

confidence: 99%

Histamine H2-receptor antagonism improves conduit artery endothelial function and reduces plasma aldosterone level without lowering arterial blood pressure in angiotensin II–hypertensive mice

Assersen,

Jensen,

Enggaard

et al. 2024

Pflugers Arch - Eur J Physiol

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Aldosterone through the mineralocorticoid receptor MR has detrimental effects on cardiovascular disease. It reduces the bioavailability of nitric oxide and impairs endothelium-dependent vasodilatation. In resistance arteries, aldosterone impairs the sensitivity of vascular smooth muscle cells to nitric oxide by promoting the local secretion of histamine which activates H2 receptors. The present experiments tested in vivo and ex vivo the hypothesis that systemic H2-receptor antagonism reduces arterial blood pressure and improves vasodilatation in angiotensin II–induced chronic hypertension. Hypertension was induced by intravenous infusion of angiotensin II (60 ng kg−1 min−1) in conscious, unrestrained mice infused concomitantly with the H2-receptor antagonist ranitidine (27.8 µg kg−1 min−1) or vehicle for 24 days. Heart rate and arterial blood pressure were recorded by indwelling arterial catheter. Resistance (mesenteric) and conductance (aortae) arteries were harvested for perfusion myography and isometric tension recordings by wire myography, respectively. Plasma was analyzed for aldosterone concentration. ANGII infusion resulted in elevated arterial blood pressure and while in vivo treatment with ranitidine reduced plasma aldosterone concentration, it did not reduce blood pressure. Ranitidine improved ex vivo endothelial function (acetylcholine 10−9 to 10−6 mol L−1) in mesenteric resistance arteries. This was abolished by ex vivo treatment with aldosterone (10−9 mol L−1, 1 h). In aortic segments, in vivo ranitidine treatment impaired relaxation. Activation of histamine H2 receptors promotes aldosterone secretion, does not affect arterial blood pressure, and protects endothelial function in conduit arteries but promotes endothelial dysfunction in resistance arteries during angiotensin II–mediated hypertension. Aldosterone contributes little to angiotensin II–induced hypertension in mice.

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“…Thereby, histamine 31 2 prevents the inhibition of NK cell functions in mixtures of monocytes and NK cells (2)(3)(4)(5)(6)(7). Results obtained in experimental animals in vivo support that histaminergic mechanisms may be important for NK cell-mediated destruction of tumour cells (8,9) and for NK cell-dependent defence against viral infection (10).…”

Section: Introductionmentioning

confidence: 90%

NK cell‐mediated killing of AML blasts: role of histamine, monocytes and reactive oxygen metabolites

Brüne

Hansson

Mellqvist

et al. 1996

European J of Haematology

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Blasts recovered from patients with acute myelogenous leukaemia (AML) were lysed by heterologous natural killer (NK) cells treated with NK cell‐activating cytokines such as interleukin‐2 (IL‐2) or interferon‐α (IFN‐α). The cytokine‐induced killing of AML blasts was inhibited by monocytes, recovered from peripheral blood by counterflow centrifugal elutriation. Histamine, at concentrations exceeding 0.1 μM, abrogated the monocyte‐induced inhibition of NK cells; thereby, histamine and IL‐2 or histamine and IFN‐α synergistically induced NK cell‐mediated destruction of AML blasts. The effect of histamine was completely blocked by the histamine H2‐receptor (H2R) antagonist ranitidine but not by its chemical control AH20399AA. Catalase, a scavenger of reactive oxygen metabolites (ROM), reversed the monocyte‐induced inhibition of NK cell‐mediated killing of blast cells, indicating that the inhibitory signal was mediated by products of the respiratory burst of monocytes. It is concluded that (i) monocytes inhibit anti‐leukemic properties of NK cells, (ii) the inhibition is conveyed by monocyte‐derived ROM, and (iii) histamine reverses the inhibitory signal and, thereby, synergizes with NK cell‐activating cytokines to induce killing of AML blasts.

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Role of histamine in natural killer cell-dependent protection against herpes simplex virus type 2 infection in mice

Cited by 6 publications

References 20 publications

Histaminergic Regulation of Natural Killer Cell‐Mediated Clearance of Tumour Cells in Mice

Histaminergic Regulation of Natural Killer Cell‐Mediated Clearance of Tumour Cells in Mice

Histamine H2-receptor antagonism improves conduit artery endothelial function and reduces plasma aldosterone level without lowering arterial blood pressure in angiotensin II–hypertensive mice

NK cell‐mediated killing of AML blasts: role of histamine, monocytes and reactive oxygen metabolites

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