Allergic Bronchospasm and Airway Hyperreactivity in the Guinea Pig

Hoshiko, Ken-ichiro; Morley, John E.

doi:10.1254/jjp.63.151

Cited by 18 publications

(7 citation statements)

References 17 publications

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“…Excepting for diminished responses to LTC4 (reduced to 41 cm H2O/L/S, i.e. by 80%), closely similar values were recorded in normal animals after an interval (1 h) indicating that such measurements are sensitive detectors of changed airway reactivity [28].…”

Section: Differences In Basal Reactivity To Test Spasmogenssupporting

confidence: 67%

Heterogeneity of airway hyperresponsiveness

CROWTHER¹,

CHAPMAN²,

MORLEY³

1997

Clin Exp Allergy

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Section: Differences In Basal Reactivity To Test Spasmogenssupporting

confidence: 67%

Heterogeneity of airway hyperresponsiveness

CROWTHER¹,

CHAPMAN²,

MORLEY³

1997

Clin Exp Allergy

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“…Although we did not determine this at the higher concentration of cetirizine more than 10 -6 g/ml (2.2 ! 10 -6 mol/l), the discrepancy between two drugs might be based on the difference of antihistamine effect: ketotifen is a non-competitive histamine antagonist in contrast to cetirizine, a competitive antihistamine [17,18]. In addition to our findings, a recent report showed that ketotifen at concentrations of 10 -6 and 10 -5 mol/l enhanced eosinophil peroxidase release induced not by fMLP but by C5a [19].…”

Section: Discussionsupporting

confidence: 48%

Effect of Ketotifen on the Production of Reactive Oxygen Species from Human Eosinophils Primed by Eotaxin

Yamada

Sannohe²,

Saito³

et al. 2003

Pharmacology

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Ketotifen is an antiallergic drug and may have direct inhibitory effects on eosinophils. To investigate the anti-eosinophilic effect of ketotifen, we examined the effect of ketotifen on the production of reactive oxygen species (ROS) from eotaxin-primed human eosinophils. Ketotifen at 10^–10–10^–6 mol/l significantly reduced the production of ROS evoked by A23187 from eosinophils primed by eotaxin. In contrast, ketotifen at 10^–5 mol/l significantly augmented the production in the absence of eotaxin. We demonstrated that appropriate concentrations of ketotifen may have direct inhibitory effects on eosinophil oxidative metabolism primed by eotaxin. Ketotifen may contribute to the treatment of allergic disease through its anti-eosinophilic effects.

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“…Airway sensitivity to histamine was not increased in our model, which is consistent with the studies cited earlier, which show that allergen challenge is required before AHR to histamine can be documented. This heterogeneity of AHR is well established and is characteristic of asthma ( O’Connor et al ., 1999 ) and animal models of hyper‐responsiveness ( Hoshiko & Morley, 1993 ).…”

Section: Discussionmentioning

confidence: 99%

Mechanism of adenosine‐induced airways obstruction in allergic guinea pigs

Keir

Boswell-Smith

Spina

et al. 2006

British J Pharmacology

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1 Inhaled adenosine induces airway obstruction in asthmatic but not healthy subjects, a phenomenon that is also observed in various animal species when they are immunised to a relevant antigen, but which does not occur in naı¨ve animals. The purpose of this study was to investigate the mechanisms of airway responsiveness to adenosine receptor agonists in anaesthetised allergic guinea pigs. 2 Inhaled adenosine 5 0 -monophosphate (AMP), the A 1 -selective adenosine receptor agonist N 6 -cyclopentyladenosine (CPA) and ovalbumin all caused airway obstruction in allergic guinea pigs, but not naı¨ve animals, as assessed by changes in total lung resistance. In contrast, the A 2a -selective (CGS 21680; 2-p-(2-carboxyethyl)phenethylamino-5 0 -N-ethylcarboxoamido adenosine) and A 3 -selective (IB-adenosine receptor agonists failed to elicit airway obstruction in passively sensitised guinea pigs. 3 Airway obstruction induced by AMP or CPA was not inhibited by the H 1 receptor antagonist, mepyramine (1 mg kg À1 ) in passively sensitised guinea-pigs. In contrast, airway obstruction to ovalbumin was significantly inhibited by this antagonist. 4 Airway obstruction induced by AMP and CPA was significantly inhibited in sensitised animals chronically treated with capsaicin. In contrast, airway obstruction to ovalbumin was not inhibited by this treatment. 5 Airway obstruction induced by AMP, CPA and ovalbumin was significantly inhibited following bilateral vagotomy or pharmacological treatment with atropine (2 mg kg À1 ). 6 Airway obstruction to CPA was inhibited by the adenosine A 1 receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX: 0.1-1 mg kg À1 ). In contrast, airway obstruction to ovalbumin was not inhibited by this treatment. 7 These observations provide evidence indicating that AMP and CPA may induce airway obstruction in sensitised guinea pigs by a mechanism unrelated to histamine release from mast cells, but is mediated via an adenosine A 1 -receptor-dependent mechanism. The inhibition of AMP-and CPA-induced airway obstruction by atropine, capsaicin and bilateral vagotomy suggests a neuronaldependent mechanism with the particular involvement of capsaicin-sensitive nerves.

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Allergic Bronchospasm and Airway Hyperreactivity in the Guinea Pig

Cited by 18 publications

References 17 publications

Heterogeneity of airway hyperresponsiveness

Heterogeneity of airway hyperresponsiveness

Effect of Ketotifen on the Production of Reactive Oxygen Species from Human Eosinophils Primed by Eotaxin

Mechanism of adenosine‐induced airways obstruction in allergic guinea pigs

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