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Characterization of allergen-induced bronchial hyperresponsiveness and airway inflammation in actively sensitized brown-Norway rats.

https://arctichealth.org/en/permalink/ahliterature57758
Source
J Allergy Clin Immunol. 1991 Dec;88(6):951-60
Publication Type
Article
Date
Dec-1991
Author
W. Elwood
J O Lötvall
P J Barnes
K F Chung
Author Affiliation
Department of Thoracic Medicine, National Heart and Lung Institute, London, England.
Source
J Allergy Clin Immunol. 1991 Dec;88(6):951-60
Date
Dec-1991
Language
English
Publication Type
Article
Keywords
Acetylcholine - administration & dosage
Aerosols
Airway Resistance - drug effects
Allergens - administration & dosage - immunology
Animals
Bronchial Hyperreactivity - etiology - immunology
Bronchial Provocation Tests - methods
Bronchitis - etiology - immunology
Bronchoalveolar Lavage Fluid - cytology
Comparative Study
Dose-Response Relationship, Immunologic
Immunization - methods
Male
Rats - immunology
Research Support, Non-U.S. Gov't
Time Factors
Abstract
Bronchial responsiveness to inhaled acetylcholine (ACh) and inflammatory cell recruitment in bronchoalveolar lavage fluid (BALF) were studied in inbred Brown-Norway rats actively sensitized to, and later exposed to, ovalbumin (OA). We examined animals 21 days after initial sensitization at 18 to 24 hours, or 5 days after a single challenge, or after the last of seven repeated exposures administered every 3 days. BALF was examined as an index of inflammatory changes within the lung. Animals repeatedly exposed to OA aerosols had an increased baseline lung resistance and a significant increase in bronchial responsiveness to inhaled ACh compared to control animals at both 18 to 24 hours and 5 days after the last OA exposure. Sensitized animals receiving a single OA aerosol also demonstrated bronchial hyperresponsiveness (BHR) to inhaled ACh (p less than 0.01) at 18 to 24 hours of a similar order as the multiple-exposed group. There was a significant increase in eosinophils, lymphocytes, and neutrophils in BALF at 18 to 24 hours but not at 5 days after single or multiple exposure to OA aerosol in the sensitized groups. Control animals demonstrated no changes in bronchial responsiveness, although a small but significant increase in inflammatory cells was observed compared to saline-only treated animals. There was a significant correlation between bronchial responsiveness and eosinophil counts in the BALF in the single allergen-exposed group (Rs = 0.68; p less than 0.05). We conclude that (1) BHR after allergen exposure in sensitized rats is associated with the presence of pulmonary inflammation but persists despite the regression of inflammatory cells in BALF after multiple OA exposures, and (2) this rat model has many characteristics of human allergen-induced BHR.
PubMed ID
1744366 View in PubMed
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Contribution of intercellular-adhesion molecule-1 in allergen-induced airway hyperresponsiveness and inflammation in sensitised brown-Norway rats.

https://arctichealth.org/en/permalink/ahliterature15953
Source
Int Arch Allergy Immunol. 1994 Jul;104(3):291-5
Publication Type
Article
Date
Jul-1994
Author
J. Sun
W. Elwood
A. Haczku
P J Barnes
P G Hellewell
K F Chung
Author Affiliation
Department of Thoracic Medicine, National Heart and Lung Institute, London, UK.
Source
Int Arch Allergy Immunol. 1994 Jul;104(3):291-5
Date
Jul-1994
Language
English
Publication Type
Article
Keywords
Allergens - immunology
Animals
Asthma - immunology - prevention & control
Bronchial Hyperreactivity - immunology - prevention & control
Bronchial Provocation Tests
Bronchoalveolar Lavage Fluid - cytology
Cell Adhesion Molecules - immunology
Eosinophils - immunology
Female
Inflammation - pathology
Intercellular Adhesion Molecule-1
Leukocyte Count
Lymphocytes - immunology
Ovalbumin
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Abstract
We investigated the potential role of intercellular-adhesion molecule-1 (ICAM-1) in allergen-induced bronchial hyperresponsiveness (BHR) and inflammation in sensitised Brown-Norway rats. Rats were sensitised with ovalbumin (OA) intraperitoneally and 21 days later they were either exposed to 0.9% NaCl or 1% OA aerosol for 15 min. Rats exposed to OA aerosol were pretreated either with ICAM-1 antibody (3 mg/kg i.p. and i.v., 45 min prior to OA exposure) or with the diluent for the antibody. Eighteen to twenty-four hours after OA or 0.9% NaCl exposure, rats were anaesthetised, tracheostomised and mechanically ventilated, and airway responsiveness to acetylcholine (ACh) aerosol was measured as the provocative concentration of ACh needed to increase pulmorary resistance by 100% (PC100). Mean -log PC100 was increased in rats exposed to OA but pretreated with diluent (2.75 +/- 0.06) compared to rats treated with ICAM-1 antibody (2.51 +/- 0.08;
PubMed ID
7913357 View in PubMed
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Effect of dexamethasone and cyclosporin A on allergen-induced airway hyperresponsiveness and inflammatory cell responses in sensitized Brown-Norway rats.

https://arctichealth.org/en/permalink/ahliterature16053
Source
Am Rev Respir Dis. 1992 Jun;145(6):1289-94
Publication Type
Article
Date
Jun-1992
Author
W. Elwood
J O Lötvall
P J Barnes
K F Chung
Author Affiliation
Department of Thoracic Medicine, National Heart and Lung Institute, London, United Kingdom.
Source
Am Rev Respir Dis. 1992 Jun;145(6):1289-94
Date
Jun-1992
Language
English
Publication Type
Article
Keywords
Acetylcholine - diagnostic use
Aerosols
Animals
Bronchial Hyperreactivity - physiopathology
Bronchial Provocation Tests
Bronchoalveolar Lavage Fluid - pathology
Comparative Study
Cyclosporine - pharmacology
Dexamethasone - pharmacology
Eosinophils - immunology
Immunization
Lymphocyte Activation - drug effects
Male
Ovalbumin - immunology
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
T-Lymphocytes - immunology
Abstract
We studied the effects of dexamethasone and cyclosporin A on the airway hyperresponsiveness (AHR) and the influx of inflammatory cells into the bronchoalveolar lavage (BAL) fluid seen 18 to 24 hr after exposure to aerosolized ovalbumin in actively ovalbumin-sensitized Brown-Norway rats. Allergen exposure resulted in an approximately sevenfold increase in bronchial responsiveness to inhaled acetylcholine associated with a significant increase in eosinophils and lymphocytes in BAL fluid. Dexamethasone (0.5 mg/kg administered intraperitoneally for 3 days) abolished the AHR and the increase in eosinophil and lymphocyte counts. However, cyclosporin A at two doses (5 and 50 mg given orally for 5 days) did not significantly prevent the induction of AHR while producing a significant inhibition of the eosinophil and lymphocyte influx. Dexamethasone (0.5 mg/kg for 3 days) or cyclosporin A (5 mg/kg for 5 days) on their own had no effect on airway responsiveness. We conclude that specific inhibition of T-lymphocyte activation in this Brown-Norway rat model is not sufficient to inhibit the induction of AHR despite suppressing allergen-induced eosinophilia in BAL fluid. However, corticosteroids, which have inhibitory effects on a wider range of inflammatory cells, are more effective. Our observations are in line with the potent effect of corticosteroids in airway inflammatory conditions such as asthma.
PubMed ID
1595993 View in PubMed
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Role of cyclooxygenase and 5-lipoxygenase metabolites, platelet-activating factor and 5-hydroxytryptamine in allergen-induced airway responses in the brown Norway rat.

https://arctichealth.org/en/permalink/ahliterature11620
Source
Int Arch Allergy Immunol. 1994;103(1):67-72
Publication Type
Article
Date
1994
Author
W. Elwood
T. Sakamoto
P J Barnes
K F Chung
Author Affiliation
Department of Thoracic Medicine, National Heart and Lung Institute, London, UK.
Source
Int Arch Allergy Immunol. 1994;103(1):67-72
Date
1994
Language
English
Publication Type
Article
Keywords
Allergens - pharmacology
Animals
Arachidonate 5-Lipoxygenase - metabolism
Asthma - physiopathology
Azepines - pharmacology
Bronchial Hyperreactivity - immunology
Bronchoalveolar Lavage Fluid - cytology
Hypersensitivity, Immediate - immunology
Male
Methysergide - pharmacology
Platelet Activating Factor - antagonists & inhibitors - physiology
Prostaglandin-Endoperoxide Synthases - metabolism
Rats
Rats, Inbred BN - immunology - physiology
Research Support, Non-U.S. Gov't
Serotonin - physiology
Triazoles - pharmacology
Abstract
We determined the effects of selective inhibition of arachidonic acid metabolism via the cyclooxygenase and 5'-lipoxygenase pathways using flurbiprofen and BWA4C, respectively, of 5-hydroxytryptamine (5-HT) using methysergide and of platelet-activating factor (PAF) using WEB 2086 on the airway responses to ovalbumin (OA) aerosol in OA-sensitized Brown Norway rats. Twenty-one days after intraperitoneal injection of OA, rats were exposed to a 1% OA or saline aerosol. Only methysergide (10 mg/kg i.p.; 3 doses over 24 h) provided significant protection of the immediate response to OA. The increase in airway responsiveness to acetylcholine after OA exposure was not significantly altered by methysergide, flurbiprofen (10 mg/kg i.p.), BWA4C (50 mg/kg i.p.) and WEB 2086 (50 mg/kg i.p.) all given over 24 h prior to OA challenge. In addition, there was no effect on the increased recovery of eosinophils and lymphocytes in bronchoalveolar lavage fluid at 24 h. We conclude that 5-HT is an important mediator of the acute response to OA, but that 5-HT, lipoxygenase and cyclooxygenase products and PAF are unlikely to be involved in OA-induced airway hyperresponsiveness and inflammation in the Brown Norway rat.
PubMed ID
8260852 View in PubMed
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