Involvement of PAF in postallergic propranolol-induced bronchoconstriction in guinea-pigs

Fujimura, Masaki; Tsujiura, M.; Songur, Nejla; Myou, Shigeharu; Matsuda, Tamotsu

doi:10.1183/09031936.96.09102064

Cited by 11 publications

(12 citation statements)

References 20 publications

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“…This is one of the most widely used techniques for determining airway constriction provoked by sensitizing antigen or chemical mediators in immunological and pharmacological studies using small experimental animals [8][9][10][11][12]. This method measures "ventilation-overflow (VO)", which is the volume of air which cannot enter into an animal's lung when the respirator inflates the lung ( fig.…”

Section: Determination Of Airway Constrictionmentioning

confidence: 99%

Effects of oral hyposensitization with recombinant Der f2 on immediate airway constriction in a murine allergic model

Yasue

Yokota²,

Yuasa³

et al. 1998

Eur Respir J

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Recombinant Der f2 (rDer f2) has recently been developed as a promising allergen for the diagnosis and immunotherapy of house-dust mite allergy, and studies in immunology. The aim of the present study was to evaluate whether oral administration of rDer f2 could suppress an immediate allergic reaction in mice sensitized with mite allergen. We developed a murine allergic model that showed bronchoconstriction after inhalation of rDer f2, and studied the effect of oral administration of rDer f2 on the reaction.Seven week old male A/J mice were intranasally immunized with rDer f2 12 times. Sensitized mice showed anti-rDer f2 immunoglobulin (Ig)E production and immediate airway constriction after inhalation of 10 mg·mL -1 of rDer f2, as determined by the Konzett-Rössler method. Immunized animals were divided into three groups, and fed phosphate-buffered saline (PBS), 0.1 mg·day -1 , or 1 mg·day -1 of rDer f2 for 4 weeks, respectively. Seven days after the last feeding, the mice were examined for their immediate response.Animals fed with 1 mg·day -1 rDer f2 showed significantly reduced bronchoconstriction after inhalation of both 2 mg·mL -1 and 10 mg·mL -1 of rDer f2 compared with PBS-fed mice. Similar results were obtained when we examined mice 10 weeks after the last feeding. Reactions in the 0.1 mg·day -1 rDer f2-fed group also tended to decrease in comparison with PBS-fed animals. Plasma anti-rDer f2 IgE, IgG1, IgG2a, and IgG2b levels were not changed by feeding with rDer f2.We conclude that recombinant Der f2 exhibits both sensitizing and hyposensitizing activities in mice. rDer f2 may be useful in immunotherapy and diagnosis of housedust mite allergy. Eur Respir J 1998; 11: 144-150 To date, several clinically important allergens such as Der 1 and Der 2 have been identified in crude mite extract [1][2][3][4]. Among others, the structural gene of Der f2, one of the major mite allergens found in Dermatophagoides farinae was cloned, and the product (recombinant Der f2 (rDer f2)) shown to exhibit allergic activity in humans comparable with native Der f2 prepared from crude mite extract [5,6]. Since Der f2 has been shown to sensitize over 80% of patients with house-dust mite allergy, rDer f2 should prove useful in the diagnosis and immunotherapy of allergic asthma and rhinitis caused by house-dust mites. It should also provide a basis for research into allergies and immunology.In the present study, with special reference to the therapeutic application of rDer f2, we established a murine allergic model by intranasal or intraperitoneal injection of rDer f2 to A/J mice, which are highly responsive to Der f2 [7]. We examined the effect of oral-hyposensitization therapy with rDer f2 against the immediate bronchoconstriction in the intranasally sensitized animals because their reaction after rDer f2 inhalation was more intense than that of intraperitoneally immunized mice. Materials and methodsAntigen rDer f2, clone 1 [5], was kindly supplied by the Nikka Whisky Distilling Co., Ltd. (Chiba, Japan), and dissolved in...

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Section: Determination Of Airway Constrictionmentioning

confidence: 99%

Effects of oral hyposensitization with recombinant Der f2 on immediate airway constriction in a murine allergic model

Yasue

Yokota²,

Yuasa³

et al. 1998

Eur Respir J

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“…W e have show n that lipid mediators such as throm boxane A2, leukotrienes, and platelet activ ating factor are involved in PI B [11][12][13] , but sensory neuropeptides do not [ 14] , suggestin g an im portance of m ediator mechanism in our guinea pigs model. The present study w as conducted to elucidate the eÚ ects of bronchodilators on the PI B.…”

mentioning

confidence: 71%

“…The changes in lung resistance to in ation, de ned as the lateral pressure of the tracheal tube or pressure at the airway opening ( Pao [ cm H 2 O] ) w as measured using a pressure transducer ( M odel TP -603T, Nihon K oden Kogyo Co., L td., Tokyo, J apan) . Because we [ 15] demonstrated that the change in P ao following inhalation of leukotriene and histamine C 4 ( L TC 4 ) represented the average of the changes in pulm onary resistance and reciprocal dynam ic lung compliance, w e used change in the P ao as an overall index of the bronchial response to bronchoactiv e agents [11][12][13][14] .…”

Section: Preparation Of Animalsmentioning

confidence: 99%

Difference in Bronchoprotective Effects of Bronchodilators on Postallergic Propranolol-Induced Bronchoconstriction

Fujimura¹

1999

Experimental Lung Research

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Administration of propranolol provokes bronchoconstriction only in asthmatic patients. It is unknown whether bronchodilator therapy can prevent the propranolol-induced bronchoconstriction (PIB). We previously reported an animal model of PIB in which bronchoconstriction is caused by propranolol when inhaled 20 minutes after an antigen provocation in passively sensitized guinea pigs. Our goal was to evaluate the bronchoprotective effects of bronchodilators on the PIB in our animal model. Propranolol was inhaled 20 minutes after an antigen challenge in passively sensitized, anesthetized, and artificially ventilated guinea pigs. Atropine (5 mg/kg) and equipotent doses of salbutamol (0.6 microgram/kg) and aminophylline (25 mg/kg), which were determined by the dose-response curves for inhibition of histamine-induced bronchoconstriction, were intravenously administered 5 minutes before the propranolol inhalation. Treatment of the animals with 25 mg/kg of aminophylline, but not with 0.6 microgram/kg of salbutamol or 5 mg/kg of atropine, significantly prevented the PIB. These results show that our animal model is an experimental model of PIB which is resistant to beta 2-agonists or anticholinergics and suggest that aminophylline may be useful to prevent and treat PIB resistant to beta 2-agonists.

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“…As the change in the Pao, but not the absolute value of the Pao, represents the average of changes in the RL and 1/Cdyn when leukotriene C 4 is inhaled [17], we have used ch.anges in the Pao as an overall index of changes in airway calibre when oedema or inflammation of the lung parenchyma is negligible [9][10][11][17][18][19]. UNDW inhalation caused an acute and sharp increase in the Pao in the present study, suggesting the presence of bronchoconstriction but not airway oedema.…”

Section: Discussionmentioning

confidence: 99%

“…We previously reported a guinea-pig model of propranolol-induced bronchoconstriction [9], in which the inhalation of propranolol 20 min after antigen inhalation caused bronchoconstriction in passively sensitized guinea-pigs. Since specific inhibitors of thromboxane A 2 (TxA 2 ) [9] and platelet-activating factor (PAF) [10], but not sensory neuropeptides [11], significantly inhibited the propranolol-induced bronchoconstriction, we postulated that an allergic mediator mechanism was important in propranolol-induced bronchoconstriction.…”

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confidence: 99%

A guinea-pig model of ultrasonically nebulized distilled water-induced bronchoconstriction

Fujimura

Amemiya²,

Myou³

et al. 1997

Eur Respir J

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Ultrasonically nebulized distilled water-induced bronchoconstriction (UNDW-IB) is specific to asthma. The mechanisms underlying UNDW-IB are not fully understood, and no reproducible animal model has been reported. The purpose of this study was to develop a guinea-pig model of UNDW-IB. Ultrasonically nebulized distilled water (UNDW) was inhaled 20 min after an aerosolized antigen challenge in passively sensitized and artificially ventilated guinea-pigs. UNDW was also inhaled 5 and 20 min after 0.1 mg x mL(-1) methacholine inhalation in nonsensitized animals. In addition, 0.1 mg x kg(-1) S-1452, a thromboxane A2 antagonist, or saline was given intravenously 5 min before UNDW inhalation in sensitized animals. The inhalation of UNDW caused bronchoconstriction, when inhaled 20 min after an antigen challenge in sensitized guinea-pigs. UNDW inhalation did not produce bronchoconstriction after saline inhalation in nonsensitized or sensitized guinea-pigs, or after antigen inhalation in nonsensitized animals. Methacholine-induced bronchoconstriction did not evoke UNDW-IB. Neither did S-1452 reduce the UNDW-IB. In conclusion, the guinea-pig model of ultrasonically nebulized distilled water-induced bronchoconstriction developed in this study suggests that allergic reaction, but not bronchoconstriction, can induce bronchial hyperresponsiveness to ultrasonically nebulized distilled water, and that thromboxane A2 is not involved in ultrasonically nebulized distilled water-induced bronchoconstriction.

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Involvement of PAF in postallergic propranolol-induced bronchoconstriction in guinea-pigs

Cited by 11 publications

References 20 publications

Effects of oral hyposensitization with recombinant Der f2 on immediate airway constriction in a murine allergic model

Effects of oral hyposensitization with recombinant Der f2 on immediate airway constriction in a murine allergic model

Difference in Bronchoprotective Effects of Bronchodilators on Postallergic Propranolol-Induced Bronchoconstriction

A guinea-pig model of ultrasonically nebulized distilled water-induced bronchoconstriction

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