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Titolo:
Characterization of increased cough sensitivity after antigen challenge inguinea pigs
Autore:
Liu, Q; Fujimura, M; Tachibana, H; Myou, S; Kasahara, K; Yasui, M;
Indirizzi:
Kanazawa Univ, Sch Med, Dept Internal Med 3, Kanazawa, Ishikawa 9208641, Japan Kanazawa Univ Kanazawa Ishikawa Japan 9208641 wa, Ishikawa 9208641, Japan
Titolo Testata:
CLINICAL AND EXPERIMENTAL ALLERGY
fascicolo: 3, volume: 31, anno: 2001,
pagine: 474 - 484
SICI:
0954-7894(200103)31:3<474:COICSA>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHRONIC NONPRODUCTIVE COUGH; SYNTHETASE INHIBITOR OKY-046; ASTHMATIC SUBJECTS; BRONCHIAL RESPONSIVENESS; EOSINOPHILIC BRONCHITIS; RECEPTOR SENSITIVITY; CITRIC-ACID; AIRWAY HYPERRESPONSIVENESS; CELLULAR INFILTRATION; HYPERTONIC SALINE;
Keywords:
airway allergy; capsaicin desensitization; cough sensitivity; guinea pigs; phosphoramidon; thromboxane A2;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Fujimura, M Kanazawa Univ, Sch Med, Dept Internal Med 3, 13-1 Takara Machi, Kanazawa, Ishikawa 9208641, Japan Kanazawa Univ 13-1 Takara Machi Kanazawa Ishikawa Japan 9208641
Citazione:
Q. Liu et al., "Characterization of increased cough sensitivity after antigen challenge inguinea pigs", CLIN EXP AL, 31(3), 2001, pp. 474-484

Abstract

Background Increased sensitivity of cough reflex is a fundamental feature of bronchodilator resistant non-productive cough associated with eosinophilic tracheobronchitis. Our hypothesis is that cough sensitivity is increasedby airway allergic reaction characterized by airway eosinophilic inflammation. The aim of this study was to elucidate the hypothesis and clarify the characteristics of the increased cough sensitivity. Materials and methods Number of coughs elicited by inhalation of increasing concentrations of capsaicin (10(-8), 10(-6) and 10(-4) m) was counted 24 h after an aerosolized antigen or saline in actively sensitized or non-sensitized (naive) conscious guinea pigs and then bronchoalveolar lavage was performed. The cough response was also measured 1 day before and 1, 2, 3, 5 and 7 days after an aerosolized antigen challenge in sensitized or naive animals. In addition, effect of procaterol (0.1 mg/kg), atropine (1 or 10 mg/kg), phosphoramidon (2.5 mg/kg) given intraperitoneally 30 min before the capsaicin challenge or capsaicin desensitization on the cough response was examined. Furthermore, the thromboxane A2 (TXA2) receptor antagonist S-1452 in a dose of 0.01 or 0.1 mg/kg or vehicle (saline) was given intraperitoneally at 24 and 1 h before the measurement of cough response. Results Number of coughs caused by capsaicin was extremely increased 24 h after an antigen challenge in sensitized guinea pigs compared with a salineor an antigen challenge in naive animals or a saline challenge in sensitized animals. The increased cough response disappeared at 3-7 days after the antigen challenge. Eosinophils in bronchoalveolar lavage fluid obtained after the measurement of capsaicin-induced coughs, which was performed 24 h after the antigen challenge, were significantly increased in sensitized guinea pigs. The eosinophil count was significantly correlated to the number of capsaicin-induced coughs. Procaterol or atropine did not alter the antigen-induced increase of cough sensitivity, whereas atropine did reduce the cough response in naive animals. Phosphoramidon increased the number of capsaicin-induced coughs in naive guinea pigs but not in sensitized and antigen-challenged animals. Capsaicin desensitization decreased the cough response inboth antigen-challenged sensitized guinea pigs and naive animals. S-1452 reduced the antigen-induced increase of cough response in sensitized guinea pigs, but not in naive animals. Answer to the question Airway allergy accompanied with airway eosinophiliainduces transient increase in cough sensitivity, which is not mediated by bronchoconstriction. The increased cough sensitivity may result in part from inactivation of neutral endopeptidase and TXA2, one of the inflammatory mediators.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/02/20 alle ore 13:40:38