Inhibitory effects of azelastine hydrochloride in alcohol-induced asthma

Takao, Atsuko; Shimoda, Terufumi; Matsuse, Hiroto; Mitsuta, Kazuko; Obase, Yasushi; Asai, Satoshi; Kohno, Shigeru

doi:10.1016/s1081-1206(10)63289-9

Cited by 26 publications

(13 citation statements)

References 13 publications

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“…Azelastine is an antihistamine agent and has been shown to inhibit the release of histamine from rat mast cells after immunologic and nonimmunologic stimuli, as well as antagonize the proinflammatory effects of histamine (Chand et al 1985, Mosges & Klimek 1998, Takao et al 1999. Here, we also report that pretreatment with azelastine inhibits vascular permeability induced by inhalation aerosol of 10 6 M UCN.…”

Section: Discussionsupporting

confidence: 66%

Expression of urocortin in rat lung and its effect on pulmonary vascular permeability

Xu²,

Zhou³

et al. 2006

Journal of Endocrinology

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Urocortin (UCN), a newly identified, 40-amino-acid, corticotropin-releasing hormone (CRH) structurally related peptide, has been demonstrated to be expressed in the central nervous system and many peripheral tissues of rats and man. This study aimed to investigate the expression profile of UCN in rat lung and the effect of UCN on lung vascular permeability. The expression of UCN mRNA was detected by reverse transcriptase PCR (RT-PCR). UCN peptide was measured by immunohistochemistry and Western blot analysis. We found that both UCN mRNA and peptide were obviously expressed in rat lung. Immunohistochemistry results showed that UCN peptide is mainly expressed in bronchial epithelium mucosa and alveolar epithelium. We also found that rats receiving inhalation aerosol of UCN had a significant elevation of lung vascular permeability compared with rats receiving vehicle and ovalbumin (OVA) by the Evans blue (EB) technique. UCN aerosol inhalation resulted in obvious pulmonary congestion and edema observed under light microscope by hematoxylin and eosin (HE) staining. The nonselective peptide CRH receptor antagonist astressin markedly reduced lung vascular permeability triggered by UCN. Enhanced pulmonary vascular permeability induced by UCN was markedly inhibited by pretreatment with the mast-cell stabilizer cromolyn and histamine-1 (H 1 ) receptor antagonist azelastine respectively, but not by the leukotriene receptor antagonist montelukast. In summary, in the present study, we demonstrated for the first time that UCN is expressed in rat lung and contributes to an increase in lung vascular permeability through activation of CRH receptors. Mast cells and histamine may be involved in this effect of UCN. Peripherally produced UCN in lung may act as an autocrine and paracrine proinflammatory factor.

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Section: Discussionsupporting

confidence: 66%

Expression of urocortin in rat lung and its effect on pulmonary vascular permeability

Xu²,

Zhou³

et al. 2006

Journal of Endocrinology

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“…In our previous studies, patients showing a 20% or more decrease in the forced expiratory volume in 1 s within 2 h after ethanol challenge were considered to have alcohol-induced asthma [1, 5, 6]. Accordingly, we incubated isolated lung mast cells for 2 h. Interestingly, histamine was the only chemical mediator produced by human airway mast cells following acetaldehyde stimulation.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, a significant increase in serum acetaldehyde occurs after alcohol consumption in half of the Japanese asthmatics [5]. We have also reported the inhibitory effects of H1-blocking agents in alcohol-induced asthma [6]. Although it is likely that acetaldehyde stimulates mast cells to release histamine, the direct effects of acetaldehyde on human airway mast cells have not yet been thoroughly evaluated.…”

Section: Introductionmentioning

confidence: 99%

Acetaldehyde Induces Histamine Release from Human Airway Mast Cells to Cause Bronchoconstriction

Kawano¹,

Matsuse²,

Kondo³

et al. 2004

Int Arch Allergy Immunol

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Backgrounds: Approximately half of the Japanese asthmatics experience exacerbation of asthma after alcohol consumption. We previously reported that this phenomenon is probably caused by histamine release from mast cells by acetaldehyde stimulation. However, no reports have described the effects of acetaldehyde on human airway mast cells. The purpose of the present study was to demonstrate acetaldehyde-induced histamine release from human airway mast cells with subsequent airway smooth muscle contraction and to investigate the ensuing mechanisms. Methods: Human tissue samples were prepared from the lungs resected from patients with lung cancer. The effect of acetaldehyde on airway muscle tone and the concentration of chemical mediators released in the organ bath were measured before and after acetaldehyde stimulation. Mast cells were prepared from lung parenchyma by the immunomagnetic method and then stimulated with acetaldehyde to determine the chemical mediators released. Results: Acetaldehyde (>3 × 10^–4M) increased airway muscle tone, which was associated with a significant increase in the release of histamine, but not thromboxane B₂ or cysteinyl-leukotrienes. A histamine (H₁ receptor) antagonist completely inhibited acetaldehyde-induced bronchial smooth muscle contraction. Acetaldehyde also induced a significant histamine release from human lung mast cells and degranulation of mast cells. Conclusions: The present results strongly suggest that acetaldehyde stimulates human airway mast cells to release histamine, which may be involved in bronchial smooth muscle contraction following alcohol consumption.

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“…We previously reported that alcohol consumption exacerbates asthma in about half of the Japanese patients with asthma [17,18,19]. Acetaldehyde, a metabolite of alcohol, plays a critical role in this alcohol-induced bronchoconstriction via stimulation of mast cells/basophils to produce histamine [20].…”

Section: Introductionmentioning

confidence: 99%

Acetaldehyde at a Low Concentration Synergistically Exacerbates Allergic Airway Inflammation as an Endocrine-Disrupting Chemical and as a Volatile Organic Compound

et al. 2012

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Background: Acetaldehyde is an endocrine-disrupting chemical (EDC) and a volatile organic compound (VOC). It is also a carcinogen and teratogen that causes bronchoconstriction in a subset of asthmatics. However, the mechanism through which acetaldehyde acts as an EDC/VOC causing allergic airway inflammation remains unknown. Objectives: To determine the effects of a low concentration of acetaldehyde, which itself did not trigger airway inflammation, on extant allergic airway inflammation in a murine model of allergic asthma. Methods: We compared airway hyperresponsiveness (AHR), lung pathology, serum IgE and airway concentrations of cytokines among four groups of BALB/c mice [control, Dermatophagoides farinae(Df) allergen-sensitized (AS), intranasally acetaldehyde-injected (ALD) and AS-ALD mice]. Results: Physiological and histological differences were not evident between ALD and control mice. AS mice developed AHR and allergic airway inflammation characterized by goblet cell hyperplasia and eosinophilic infiltration. Both AHR and airway eosinophilia were significantly enhanced in AS-ALD compared with AS mice. Serum total and Df-specific IgE were significantly increased in both AS and AS-ALD mice compared with control and ALD mice, but comparable between AS and AS-ALD mice. Mite allergen sensitization significantly increased interleukin-5 and granulocyte macrophage colony-stimulating factor, and decreased interferon-γ levels in the airways; injecting acetaldehyde into airways with allergic inflammation significantly increased the levels of these inflammatory cytokines. Conclusions: Exposure to acetaldehyde can enhance allergic airway inflammation in asthma.

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Inhibitory effects of azelastine hydrochloride in alcohol-induced asthma

Cited by 26 publications

References 13 publications

Expression of urocortin in rat lung and its effect on pulmonary vascular permeability

Expression of urocortin in rat lung and its effect on pulmonary vascular permeability

Acetaldehyde Induces Histamine Release from Human Airway Mast Cells to Cause Bronchoconstriction

Acetaldehyde at a Low Concentration Synergistically Exacerbates Allergic Airway Inflammation as an Endocrine-Disrupting Chemical and as a Volatile Organic Compound

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