High concentrations of histamine stimulate equine polymorphonuclear neutrophils to produce reactive oxygen species

Benbarek, H.; Mouithys‐Mickalad, Ange; Deby‐Dupont, G.; Deby, C.; Grulke, Sigrid; Lamy, Maurice; Serteyn, Didier

doi:10.1007/s000110050509

Cited by 28 publications

(15 citation statements)

References 44 publications

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“…The precise mechanisms regulating how the stimulation of H1 receptors induces the activation of JAK2 in keratinocytes should be investigated in the future. It is reported that the stimulation of certain G-protein-coupled receptors including histamine receptors transactivates epidermal growth factor receptor (EGFR) or generates reactive oxygen species (ROS) [40,41], and that both signals can activate JAK2 [33,40,42]. However, neither the EGFR tyrosine kinase inhibitor AG1478 nor the antioxidant diphenyleneiodonium suppressed the JAK2 autophosphorylation induced by histamine in human keratinocytes (data not shown).…”

Section: Discussionmentioning

confidence: 79%

Histamine induces human β-defensin-3 production in human keratinocytes

Ishikawa

Kanda

Hau

et al. 2009

Journal of Dermatological Science

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Section: Discussionmentioning

confidence: 79%

Histamine induces human β-defensin-3 production in human keratinocytes

Ishikawa

Kanda

Hau

et al. 2009

Journal of Dermatological Science

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“…Apart from being powerful coronary vasoconstrictor, histamine can activate platelets and potentiates the aggregatory response of other agonists including adrenaline, 5-hydroxytryptamine, and thrombin [36 -38]; it modulates the activity of inflammatory cells such as neutrophils [39], monocytes [40], and eosinophils [41]. Moreover, histamine induces proinflammatory cytokine production from endothelial cells [42], upregulates Pselectin on the endothelial cell surface [43,44], and induces intimal thickening in a mouse model of thrombosis [45].…”

Section: Mast Cell Activation-degranulationmentioning

confidence: 99%

Kounis syndrome (allergic angina and allergic myocardial infarction): A natural paradigm?

Kounis¹

2006

International Journal of Cardiology

472

436

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“…6 Histamine also can activate platelets, and it potentiates the aggregatory response of other agonists including adrenaline, 5-hydroxytryptamine, and thrombin. [7][8][9] Moreover, histamine is able to modulate the activity of inflammatory cells such as neutrophils, 10 monocytes, 11 and eosinophils. 12 In urban environments, diesel exhaust particles (DEP) are one of the main contributors of atmospheric particulate matter of diameter Ͻ2.5 m (PM 2.5 ).…”

mentioning

confidence: 99%

Pharmacological Stabilization of Mast Cells Abrogates Late Thrombotic Events Induced by Diesel Exhaust Particles in Hamsters

et al. 2004

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Background-Particulate air pollution is associated with cardiovascular diseases and myocardial infarction (MI). Methods and Results-We investigated the relationship between airway inflammation and thrombosis 24 hours after intratracheal (IT) instillation of diesel exhaust particles (DEP; 50 g/hamster). Mild thrombosis was induced in the femoral vein by endothelial injury, and the consequences of airway inflammation on thrombogenicity were studied via online video microscopy. Lung inflammation and histamine analysis in bronchoalveolar lavage (BAL) and plasma were performed after pretreatment with dexamethasone (DEX) or sodium cromoglycate (SC). DEP induced airway inflammation and histamine release in BAL and in plasma, and increased thrombosis, without elevating plasma von Willebrand factor (vWF) levels. The IT instillation of 400-nm positively charged polystyrene particles (500 g/hamster), serving as particles that do not penetrate into the circulation, equally produced airway inflammation, histamine release, and enhanced thrombosis. Histamine in plasma resulted from basophil activation. Intraperitoneal (IP) pretreatment with DEX (5 mg/kg) abolished the DEP-induced histamine increase in BAL and plasma and abrogated airway inflammation and thrombogenicity. The IT pretreatment with DEX (0.5 mg/kg) showed a partial but parallel inhibition of all of these parameters. Pretreatment with SC (40 mg/kg, IP) strongly inhibited airway inflammation, thrombogenicity, and histamine release. Conclusions-Our results are compatible with the triggering of mast cell degranulation and histamine release by DEP.Histamine plays an initial central role in airway inflammation, further release of histamine by circulating basophils, and peripheral thrombotic events. Antiinflammatory pretreatment can abrogate the peripheral thrombogenicity by preventing histamine release from mast cells.

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High concentrations of histamine stimulate equine polymorphonuclear neutrophils to produce reactive oxygen species

Abstract: High concentrations of histamine stimulated the neutrophils to product ROS and free radicals via H1 receptors and the NADPH-oxidase pathway.

Cited by 28 publications

References 44 publications

Histamine induces human β-defensin-3 production in human keratinocytes

Histamine induces human β-defensin-3 production in human keratinocytes

Kounis syndrome (allergic angina and allergic myocardial infarction): A natural paradigm?

Pharmacological Stabilization of Mast Cells Abrogates Late Thrombotic Events Induced by Diesel Exhaust Particles in Hamsters

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