The effect of histamine on the oxidative burst of HL60 cells before and after exposure to reactive oxygen species

Ching, Tjong-Lie; Koelemij, J G; Bast, Aalt

doi:10.1007/bf01782018

Cited by 19 publications

(12 citation statements)

References 32 publications

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“…Although reactive oxidative metabolites may contribute to the killing of H. pylori microorganisms, they may also injure the surrounding tissue (1). The role of HDC activation and histamine generation in the response to oxidant stress of the gastrointestinal tract remains unclear, although several studies have suggested that histamine synthesized by HDC may facilitate healing of the gut mucosa (23)(24)(25) and inhibit the further generation of ROMs by neutrophils (44,45). In addition, a role in acid secretion has been suggested by recent studies showing that H 2 O 2 at low concentrations is capable of stimulating acid secretion by sevenfold in isolated gastric mucosa (46).…”

Section: Discussionmentioning

confidence: 96%

Oxidative Stress Activates the Human Histidine Decarboxylase Promoter in AGS Gastric Cancer Cells

Höcker¹,

Rosenberg²,

Xavier³

et al. 1998

Journal of Biological Chemistry

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Oxidant stress is thought to play a role in the pathogenesis of many gastric disorders. We have recently reported that histidine decarboxylase (HDC) promoter activity is stimulated by gastrin through a protein kinase C-and extracellular signal-regulating kinase (ERK)-dependent pathway in gastric cancer (AGS-B) cells, and this transcriptional response is mediated by a downstream cis-acting element, the gastrin response element (GAS-RE). To study the mechanism through which oxidant stress affects gastric cells, we examined the effects of hydrogen peroxide (H 2 O 2 ) on HDC promoter activity and intracellular signaling in AGS-B cells. H 2 O 2 (10 mM) specifically activated the HDC promoter 10 -12-fold, and this activation was blocked by both mannitol and Nacetylcysteine.

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Section: Discussionmentioning

confidence: 96%

Oxidative Stress Activates the Human Histidine Decarboxylase Promoter in AGS Gastric Cancer Cells

Höcker¹,

Rosenberg²,

Xavier³

et al. 1998

Journal of Biological Chemistry

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“…There were however, detectable amounts of h1 mRNA in mononuclear and stromal cells, in keeping with the finding of immunoregulatory control of lymphocytes by histamine binding 48 and histamine release from mast cells. 49 Additionally, the recent discovery of the h4 receptor primarily expressed in bone marrow and eosinophils, but undetected in brain tempts speculation of a peripheral immune target particularly with respect to asthma and allergy, to which clozapine has moderate affinity. 50 The current data confirm and extend on previous pharmacological 26,27 and mRNA expression studies that suggested the existence of multiple muscarinic receptors on blood lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

Potential clozapine target sites on peripheral hematopoietic cells and stromal cells of the bone marrow

et al. 2003

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The antipsychotic drug clozapine, acts via interaction with selective neurotransmitter receptor systems. Its use however, is associated with lifethreatening agranulocytosis. The mechanism by which this occurs and its possible relationship with the drug's atypicality remain unclear. As a first step in identifying mechanistic pathways involved, profiling of neurotransmitter receptors on human neutrophils, mononuclear and bone marrow stromal cells as putative targets for clozapine-mediated toxicity was undertaken. Expression of mRNA encoding dopaminergic d2, d3, d4; serotonergic 5ht2a, 5ht2c, 5ht3, 5ht6, 5ht7; adrenergic a1a, a2; histaminergic h1 and muscarinic m1, m2, m3, m4, m5 receptors was analyzed by reverse transcription-polymerase chain reaction methods. While 5ht2c, 5ht6, m1 and m2 mRNA were undetected, the presence of the other receptors indicates sites at which clozapine could bind and induce toxicity of neutrophils and stromal components which regulate granulopoiesis. The functional significance of differential receptor expression while unknown, may argue for neural regulation of hematopoiesis.

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“…This inhibitory effect on the calcium intracellular concentration in neutrophils may represent one of the mechanisms responsible for inhibition of ROS generation by these drugs. Ching et al (1995) found that 10 -3 M histamine inhibited the N-fMLP-induced superoxide anion radical production by dibutyryl cAMP-differentiated HL60 cells, a model of human neutrophils. They also showed that this effect was partly mediated via histamine H2 receptors; the histamine H2 receptor antagonists famotidine, mifentidine and ranitidine partially antagonized the inhibitory effect of histamine.…”

mentioning

confidence: 95%

Modulation of neutrophil oxidative burst via histamine receptors

Čı́ž

Lojek

2013

British J Pharmacology

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Histamine has the ability to influence the activity of immune cells including neutrophils and plays a pivotal role in inflammatory processes, which are a complex network of cellular and humoral events. One of the main functions manifested by activated neutrophils is oxidative burst, which is linked to the production of reactive oxygen species; therefore, the effects of histamine receptor agonists and antagonists on the oxidative burst of neutrophils is reviewed. A role for the well-characterized histamine H1 and H2 receptors in this process is discussed and compared to that of the recently discovered H4 receptor. LINKED ARTICLESThis article is part of a themed issue on Histamine Pharmacology Update. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2013.170.issue-1 AbbreviationsCaI, calcium ionophore A23187; N-fMLP, N-formyl-methionyl-leucyl-phenylalanine; OZP, opsonized zymosan particle; PMA, phorbol myristate acetate; ROS, reactive oxygen species; TLR, toll-like receptor Oxidative burst of neutrophilsNeutrophils are the most abundant type of white blood cells, comprising about 50-70% of all leukocytes. One of the most important defence mechanisms of neutrophils is associated with their ability to mediate a strong oxidative burst through the formation of reactive oxygen species (ROS). While oxidative burst is important for the elimination of invading microorganisms, the overproduction of ROS or the impairment of endogenous antioxidant defences may result in detrimental effects on the host's own cells and tissues (Freitas et al., 2009). Neutrophil oxidative burst is accompanied by the production of NADPH oxidase, which reduces oxygen to a superoxide anion radical. It is generally assumed that the NADPH oxidase is activated exclusively in the plasma membrane. However, in neutrophils, this assumption does not fit with the subcellular localization of the membrane components of the NADPH oxidase, which are stored in the granular compartments, and it has become increasingly evident that oxidants are also produced in an intracellular compartment, identified as specific granules. Myeloperoxidase is stored in another subset of granules, the azurophil granules, and participates in the processing of the ROS. In fact, it has been suggested that neutrophil activation is accompanied by the fusion of azurophil with specific granules, allowing these peroxidase-dependent reactions to take place (Karlsson and Dahlgren, 2002). PKC-d is required for full production of NADPH oxidase and activation of the respiratory burst. Neutrophils also express PKC-a and b, which may be involved in adhesion, degranulation and phagocytosis, but the evidence for this is not yet conclusive (Bertram and Ley, 2011). Although the complex mechanisms that coordinate the membrane traffic, oxidative burst and release of granule contents required for the microbicidal activities of neutrophils are not completely understood, it is evident that they are unique and differ from those in macrophages (Nordenfelt and Tapper, 2011). Neutr...

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The effect of histamine on the oxidative burst of HL60 cells before and after exposure to reactive oxygen species

Cited by 19 publications

References 32 publications

Oxidative Stress Activates the Human Histidine Decarboxylase Promoter in AGS Gastric Cancer Cells

Oxidative Stress Activates the Human Histidine Decarboxylase Promoter in AGS Gastric Cancer Cells

Potential clozapine target sites on peripheral hematopoietic cells and stromal cells of the bone marrow

Modulation of neutrophil oxidative burst via histamine receptors

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