The role of histamine in allergic diseases

White, Martha V.

doi:10.1016/s0091-6749(05)80223-4

Cited by 287 publications

(174 citation statements)

References 10 publications

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“…Its main sources are basophils and mast cells, which are distributed throughout the body and are well known for their roles in allergic disorders and inflammation (1). Histamine has been involved in allergic reactions, vasodilatation and vasoconstriction, gastric acid secretion, and neurotransmission (2)(3)(4). In addition to its proinflammatory actions (5,6), histamine possesses anti-inflammatory and immunosuppressive effects (7).…”

Section: Importance Of Histamine In the Cytokine Network In The Lung mentioning

confidence: 99%

Importance of Histamine in the Cytokine Network in the Lung Through H2 and H3 Receptors: Stimulation of IL-10 Production

Sirois

Ménard

Moses

et al. 2000

The Journal of Immunology

105

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Histamine, a well-known inflammatory mediator, has been implicated in various immunoregulatory effects that are poorly understood. Thus, we tested the hypothesis that histamine inhibits the release of a proinflammatory cytokine, namely TNF, by stimulating the release of an anti-inflammatory cytokine, IL-10. Alveolar macrophages (AMs) from humans, Sprague Dawley rats, and the AM cell line, NR8383, were treated with different concentrations of histamine (10−5-10−7 M) for 2 h prior to their stimulation with suboptimal concentration of LPS (1 ng/ml) for 4 h. Histamine inhibited TNF release in a dose-dependent manner. This inhibition was mimicked by H2 and H3 receptor agonists, but not by H1 receptor agonist. Furthermore, we demonstrated the expression of H3 receptor mRNA in human AMs. Interestingly, treatment of AMs with anti-IL-10, anti-PGE2, or a NO synthase inhibitor (Nω-nitro-l-arginine methyl ester) before the addition of histamine abrogated the inhibitory effect of the latter on TNF release. Histamine treatment (10−5 M) increased the release of IL-10 from unstimulated (2.2-fold) and LPS-stimulated (1.7-fold) AMs. Unstimulated AMs, NR8383, express few copies of IL-10 mRNA, as tested by quantitative PCR, but expression of IL-10 was increased by 1.5-fold with histamine treatment. Moreover, the stimulation of IL-10 release by histamine was abrogated by pretreatment with anti-PGE2 or the NO synthase inhibitor, Nω-nitro-l-arginine methyl ester. Thus, histamine increases the synthesis and release of IL-10 from AMs through PGE2 and NO production. These results suggest that histamine may play an important role in the modulation of the cytokine network.

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Section: Importance Of Histamine In the Cytokine Network In The Lung mentioning

confidence: 99%

Importance of Histamine in the Cytokine Network in the Lung Through H2 and H3 Receptors: Stimulation of IL-10 Production

Sirois

Ménard

Moses

et al. 2000

The Journal of Immunology

105

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“…Histamine exerts a variety of proinflammatory and immunomodulating effects through the interaction with three receptors, H 1 , H 2 , and H 3 (6,7). The pivotal role of histamine in allergic inflammation is supported also by the observation that antagonists of the H 1 receptor are effective in alleviating some of the acute symptoms of allergic disorders (8). The immediate actions of histamine on vascular endothelium and on bronchial and vascular smooth muscle cells have been clearly elucidated.…”

mentioning

confidence: 99%

“…The immediate actions of histamine on vascular endothelium and on bronchial and vascular smooth muscle cells have been clearly elucidated. These effects are mostly mediated by the activation of the H 1 receptor, and they are responsible for the majority of the acute symptoms in bronchial asthma, allergic rhinitis, and urticaria (8). Histamine also exerts a variety of other regulatory functions by modulating the activity of T cells (9,10), monocytes (11), neutrophils (12), and eosinophils (13).…”

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confidence: 99%

Histamine Induces Exocytosis and IL-6 Production from Human Lung Macrophages Through Interaction with H1 Receptors

Triggiani

Gentile

Secondo

et al. 2001

The Journal of Immunology

135

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Increasing evidence suggests that a continuous release of histamine from mast cells occurs in the airways of asthmatic patients and that histamine may modulate functions of other inflammatory cells such as macrophages. In the present study histamine (10−9–10−6 M) increased in a concentration-dependent fashion the basal release of β-glucuronidase (EC50 = 8.2 ± 3.5 × 10−9 M) and IL-6 (EC50 = 9.3 ± 2.9 × 10−8 M) from human lung macrophages. Enhancement of β-glucuronidase release induced by histamine was evident after 30 min and peaked at 90 min, whereas that of IL-6 required 2–6 h of incubation. These effects were reproduced by the H1 agonist (6-[2-(4-imidazolyl)ethylamino]-N-(4-trifluoromethylphenyl)heptane carboxamide but not by the H2 agonist dimaprit. Furthermore, histamine induced a concentration-dependent increase of intracellular Ca2+ concentrations ([Ca2+]i) that followed three types of response, one characterized by a rapid increase, a second in which [Ca2+]i displays a slow but progressive increase, and a third characterized by an oscillatory pattern. Histamine-induced β-glucuronidase and IL-6 release and [Ca2+]i elevation were inhibited by the selective H1 antagonist fexofenadine (10−7–10−4 M), but not by the H2 antagonist ranitidine. Inhibition of histamine-induced β-glucuronidase and IL-6 release by fexofenadine was concentration dependent and displayed the characteristics of a competitive antagonism (Kd = 89 nM). These data demonstrate that histamine induces exocytosis and IL-6 production from human macrophages by activating H1 receptor and by increasing [Ca2+]i and they suggest that histamine may play a relevant role in the long-term sustainment of allergic inflammation in the airways.

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“…Metabolism of antihistamines and drug interaction are given in Table 2. Antagonists of H1 receptors are used in treatment of allergic rhinoconjuctivitis and relieve sneezing nasal and ocular itching, rhinorrhea, conjujctival erythema and early phase of inflammatory response, but they are less effective in the treatment of late phase of inflammatory response (64).…”

Section: A Nt I Hi St a M I Nesmentioning

confidence: 99%