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Adoptive transfer of allergen-specific CD4+ T cells induces airway inflammation and hyperresponsiveness in brown-Norway rats.

https://arctichealth.org/en/permalink/ahliterature57604
Source
Immunology. 1997 Jun;91(2):176-85
Publication Type
Article
Date
Jun-1997
Author
A. Haczku
P. Macary
T J Huang
H. Tsukagoshi
P J Barnes
A B Kay
D M Kemeny
K F Chung
R. Moqbel
Author Affiliation
Department of Allergy and Clinical Immunology, Guy's Hospital, London, UK.
Source
Immunology. 1997 Jun;91(2):176-85
Date
Jun-1997
Language
English
Publication Type
Article
Keywords
Adoptive Transfer
Animals
Bronchial Hyperreactivity - immunology
Bronchoalveolar Lavage Fluid - immunology
CD4-Positive T-Lymphocytes - immunology - transplantation
CD8-Positive T-Lymphocytes - immunology - transplantation
Cell Culture Techniques
Cell Division - immunology
Eosinophils - immunology
Leukocyte Count
Lymphocyte Transfusion
Male
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Spleen - immunology
Abstract
Following allergen exposure, sensitized Brown-Norway rats develop airway hyperresponsiveness (AHR) and eosinophilic inflammation together with an increase in activated T cells (CD25+) in the airways. We tested the hypothesis that CD4+ T cells are involved directly in the acquisition of AHR. Spleen T cells from animals that were injected intraperitoneally on three consecutive days with ovalbumin/Al(OH)3, showed a dose-dependent proliferative response in vitro to ovalbumin, but not to bovine serum albumin, as measured by [3H]thymidine uptake. For total T-cell transfer, spleen cells obtained from donor rats 4 days after sensitization were depleted of adherent cells by a nylon wool column separation. CD4+ and CD8+ T cells were purified by immunomagnetic beads cell separation. Recipient naive rats were injected intravenously with 50 x 10(6) total T cells, 20 x 10(6) and 5 x 10(6) CD4+ cells, and 5 x 10(6) CD8+ cells, and were exposed to ovalbumin aerosol 24 hr afterwards. After a further 24 hr, airway responsiveness to acetylcholine (ACh) was measured and provocative concentration (PC) values PC100, PC200 and PC300) (the ACh concentration needed to achieve 100, 200 and 300% increase in lung resistance above baseline) were calculated. Airway responsiveness was significantly increased in recipients of sensitized total T cells compared with recipients of cells from saline-injected donor rats (P
PubMed ID
9227314 View in PubMed
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Adoptive transfer of allergic airway responses with sensitized lymphocytes in BN rats.

https://arctichealth.org/en/permalink/ahliterature57674
Source
Am J Respir Crit Care Med. 1995 Jul;152(1):64-70
Publication Type
Article
Date
Jul-1995
Author
A. Watanabe
P. Rossi
P M Renzi
L J Xu
R D Guttmann
J G Martin
Author Affiliation
Meakins-Christie Laboratories, McGill University, Royal Victoria Hospital, Montreal, Quebec, Canada.
Source
Am J Respir Crit Care Med. 1995 Jul;152(1):64-70
Date
Jul-1995
Language
English
Publication Type
Article
Keywords
Animals
Bronchial Hyperreactivity - immunology - physiopathology
Bronchial Provocation Tests
Bronchoalveolar Lavage Fluid - cytology
Eosinophils - immunology
Immunoglobulin E - immunology
Immunotherapy, Adoptive
Male
Ovalbumin - immunology
Passive Cutaneous Anaphylaxis - immunology
Rats
Rats, Inbred BN
Rats, Sprague-Dawley
Research Support, Non-U.S. Gov't
Respiratory Hypersensitivity - immunology - physiopathology
Serum Albumin, Bovine - immunology
T-Lymphocytes - immunology
Abstract
To evaluate the role of lymphocytes in the pathogenesis of allergic bronchoconstriction, we investigated whether allergic airway responses are adoptively transferred by antigen-primed lymphocytes in Brown Norway (BN) rats. Animals were actively sensitized to ovalbumin (OA) or sham sensitized, and 14 d later mononuclear cells (MNCs) were isolated from intrathoracic lymph nodes, passed through a nylon wool column, and transferred to naive syngeneic rats. Recipients were challenged with aerosolized OA or bovine serum albumin (BSA) (5% wt/vol) and analyzed for changes in lung resistance (RL), airway responsiveness to inhaled methacholine (MCh), and bronchoalveolar lavage (BAL) cells. Recipients of MNCs from sensitized rats responded to OA inhalation and exhibited sustained increases in RL throughout the 8-h observation period, but without usual early airway responses. Recipients of sham-sensitized MNCs or BSA-challenged recipients failed to respond to antigen challenge. At 32 h after OA exposure, airway responsiveness to MCh was increased in four of seven rats that had received sensitized MNCs (p = 0.035). BAL eosinophils increased at 32 h in the recipients of both sensitized and sham-sensitized MNCs. However, eosinophil numbers in BAL were inversely correlated with airway responsiveness in the recipients of sensitized MNCs (r = -0.788, p = 0.036). OA-specific immunoglobulin E (IgE) was undetectable by enzyme-linked immunosorbent assay (ELISA) or passive cutaneous anaphylaxis (PCA) in recipient rats following adoptive transfer. In conclusion, allergic late airway responses (LAR) and cholinergic airway hyperresponsiveness, but not antigen-specific IgE and early responses, were adoptively transferred by antigen-primed lymphocytes in BN rats.(ABSTRACT TRUNCATED AT 250 WORDS)
PubMed ID
7599864 View in PubMed
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Airway hyperresponsiveness, elevation of serum-specific IgE and activation of T cells following allergen exposure in sensitized Brown-Norway rats.

https://arctichealth.org/en/permalink/ahliterature15906
Source
Immunology. 1995 Aug;85(4):598-603
Publication Type
Article
Date
Aug-1995
Author
A. Haczku
K F Chung
J. Sun
P J Barnes
A B Kay
R. Moqbel
Author Affiliation
Department of Allergy and Clinical Immunology, National Heart and Lung Institute, London, UK.
Source
Immunology. 1995 Aug;85(4):598-603
Date
Aug-1995
Language
English
Publication Type
Article
Keywords
Allergens - immunology
Animals
Bronchial Hyperreactivity - immunology
Bronchial Provocation Tests
Bronchoalveolar Lavage Fluid - immunology
Female
Immunoglobulin E - blood
Lymphocyte Activation - immunology
Ovalbumin - immunology
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
T-Lymphocyte Subsets - immunology
Abstract
T lymphocytes may play a regulatory role in the development of allergic airway hyperresponsiveness (AHR). We have studied the relationship between airway responsiveness and a number of immunological changes in Brown-Norway rats sensitized intraperitoneally and repeatedly exposed to ovalbumin (OVA) aerosol. Acetylcholine provocation concentration (PC)150 (the concentration of acetylcholine causing a 150% increase of base-line lung resistance) was measured and peripheral blood and bronchoalveolar lavage (BAL) cells were collected 18-24hr after the final exposure. Total and OVA-specific IgE in serum was measured by enzyme-linked immunosorbent assay (ELISA). Mononuclear cells were analysed by flow cytometry after labelling with monoclonal antibodies against CD2 (pan T-cell marker), CD4, CD8 (T-cell subsets) or CD25 (interleukin-2 receptor). There were significant differences in PC150 (P
PubMed ID
7558155 View in PubMed
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Airway hyperresponsiveness to bradykinin induced by allergen challenge in actively sensitised Brown Norway rats.

https://arctichealth.org/en/permalink/ahliterature15208
Source
Naunyn Schmiedebergs Arch Pharmacol. 2004 Feb;369(2):166-78
Publication Type
Article
Date
Feb-2004
Author
K M Ellis
C. Cannet
L. Mazzoni
J R Fozard
Author Affiliation
Research Department, Novartis Institute for Biomedical Research, 4002 Basel, Switzerland.
Source
Naunyn Schmiedebergs Arch Pharmacol. 2004 Feb;369(2):166-78
Date
Feb-2004
Language
English
Publication Type
Article
Keywords
Adenosine - pharmacology
Animals
Arachidonate 5-Lipoxygenase - physiology
Bradykinin - pharmacology - physiology
Bronchial Hyperreactivity - immunology - physiopathology
Bronchoconstriction - drug effects
Bronchoconstrictor Agents - pharmacology
Comparative Study
Disease Models, Animal
Endopeptidases - physiology
Lung - pathology
Male
Mast Cells - physiology
Methacholine Chloride - pharmacology
Ovalbumin - immunology
Rats
Rats, Inbred BN
Receptors, Adrenergic, beta-1 - agonists
Receptors, Adrenergic, beta-2 - antagonists & inhibitors
Receptors, Muscarinic - physiology
Tachykinins - physiology
Abstract
The mechanism(s) of bradykinin-induced bronchoconstriction was investigated in the Brown Norway (BN) rat model of allergic asthma. Bronchoconstrictor responses to i.v. bradykinin in BN rats were maximally augmented 24 h following challenge with allergen and declined at later time points. Histological evaluation of the inflammatory status of the lungs after ovalbumin (OA) challenge showed a marked inflammatory response, which was maximal at 24 h and declined thereafter. However, pretreatment with budesonide did not inhibit the augmented bronchoconstrictor response to bradykinin 24 h after allergen challenge. The selective B1 receptor agonist, Lys-[desArg9]-BK had no bronchoconstrictor effects, whereas the selective B2 receptor antagonist, HOE 140, abolished the response to bradykinin in OA-challenged animals. The augmented response to bradykinin was not affected by methysergide, indomethacin, disodium cromoglycate, iralukast, the 5-lipoxygenase inhibitor, CGS8515, or the NK2 receptor antagonist, SR48968. It was, however, partially inhibited by atropine both in saline- and OA-challenged animals. Pretreatment with captopril and thiorphan markedly potentiated responses to bradykinin both in saline- and OA-challenged animals. Thus, augmentation of the bronchoconstrictor response to bradykinin occurs in actively sensitised BN rats 24 h after challenge with OA and is associated with marked pulmonary inflammation. The response is entirely B2 receptor mediated and approximately 50% of the response is cholinergic. However, mast cell activation, the products of the cyclooxygenase or 5-lipoxygenase pathways and tachykinins are not involved. Peptidase inhibition mimics the effect of allergen challenge on the bronchoconstrictor response to bradykinin and it remains possible that the mechanism of the augmented response to bradykinin following allergen challenge involves downregulation of peptidase activity as a consequence of the inflammatory response.
PubMed ID
14727005 View in PubMed
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Allergen-specific Th1 cells counteract efferent Th2 cell-dependent bronchial hyperresponsiveness and eosinophilic inflammation partly via IFN-gamma.

https://arctichealth.org/en/permalink/ahliterature15527
Source
J Immunol. 2001 Jan 1;166(1):207-17
Publication Type
Article
Date
Jan-1-2001
Author
T J Huang
P A MacAry
P. Eynott
A. Moussavi
K C Daniel
P W Askenase
D M Kemeny
K F Chung
Author Affiliation
Thoracic Medicine, National Heart and Lung Institute, Imperial College School of Medicine, London, United Kingdom.
Source
J Immunol. 2001 Jan 1;166(1):207-17
Date
Jan-1-2001
Language
English
Publication Type
Article
Keywords
Administration, Inhalation
Adoptive Transfer
Allergens - administration & dosage - immunology
Animals
Antibodies, Monoclonal - administration & dosage
Bronchial Hyperreactivity - immunology - pathology - prevention & control
Bronchoalveolar Lavage Fluid - immunology
Cell Line
Epitopes, T-Lymphocyte - administration & dosage - immunology
Inflammation - immunology - pathology - prevention & control
Injections, Intravenous
Interferon Type II - immunology - physiology
Interleukin-4 - antagonists & inhibitors - genetics
Lung - cytology - immunology
Male
Ovalbumin - administration & dosage - immunology
Pulmonary Eosinophilia - immunology - pathology - prevention & control
RNA, Messenger - antagonists & inhibitors
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Th1 Cells - immunology - transplantation
Th2 Cells - immunology - transplantation
Abstract
Th2 T cell immune-driven inflammation plays an important role in allergic asthma. We studied the effect of counterbalancing Th1 T cells in an asthma model in Brown Norway rats that favors Th2 responses. Rats received i.v. transfers of syngeneic allergen-specific Th1 or Th2 cells, 24 h before aerosol exposure to allergen, and were studied 18-24 h later. Adoptive transfer of OVA-specific Th2 cells, but not Th1 cells, and OVA, but not BSA exposure, induced bronchial hyperresponsiveness (BHR) to acetylcholine and eosinophilia in a cell number-dependent manner. Importantly, cotransfer of OVA-specific Th1 cells dose-dependently reversed BHR and bronchoalveolar lavage (BAL) eosinophilia, but not mucosal eosinophilia. OVA-specific Th1 cells transferred alone induced mucosal eosinophilia, but neither BHR nor BAL eosinophilia. Th1 suppression of BHR and BAL eosinophilia was allergen specific, since cotransfer of BSA-specific Th1 cells with the OVA-specific Th2 cells was not inhibitory when OVA aerosol alone was used, but was suppressive with OVA and BSA challenge. Furthermore, recipients of Th1 cells alone had increased gene expression for IFN-gamma in the lungs, while those receiving Th2 cells alone showed increased IL-4 mRNA. Importantly, induction of these Th2 cytokines was inhibited in recipients of combined Th1 and Th2 cells. Anti-IFN-gamma treatment attenuated the down-regulatory effect of Th1 cells. Allergen-specific Th1 cells down-regulate efferent Th2 cytokine-dependent BHR and BAL eosinophilia in an asthma model via mechanisms that depend on IFN-gamma. Therapy designed to control the efferent phase of established asthma by augmenting down-regulatory Th1 counterbalancing mechanisms should be effective.
PubMed ID
11123294 View in PubMed
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Antigen-induced airway inflammation in the Brown Norway rat results in airway smooth muscle hyperplasia.

https://arctichealth.org/en/permalink/ahliterature15325
Source
J Appl Physiol. 2002 Nov;93(5):1833-40
Publication Type
Article
Date
Nov-2002
Author
K F Xu
R. Vlahos
A. Messina
T L Bamford
J F Bertram
A G Stewart
Author Affiliation
Bernard O'Brien Institute of Microsurgery, St. Vincent's Hospital, Fitzroy, Victoria 3065, Australia.
Source
J Appl Physiol. 2002 Nov;93(5):1833-40
Date
Nov-2002
Language
English
Publication Type
Article
Keywords
Acetylcholine - pharmacology
Airway Resistance
Animals
Bronchi - drug effects - pathology
Bronchial Hyperreactivity - immunology - physiopathology
Bronchitis - immunology - pathology - physiopathology
Cell Count
Hyperplasia
Hypersensitivity, Immediate - immunology - physiopathology
Male
Muscle, Smooth - pathology
Ovalbumin - immunology
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Abstract
Asthma is characterized by chronic airways inflammation, airway wall remodeling, and airway hyperresponsiveness (AHR). An increase in airway smooth muscle has been proposed to explain a major part of AHR in asthma. We have used unbiased stereological methods to determine whether airway smooth muscle hyperplasia and AHR occurred in sensitized, antigen-challenged Brown Norway (BN) rats. Ovalbumin (OA)-sensitized BN rats chronically exposed to OA aerosol displayed airway inflammation and a modest level of AHR to intravenously administered ACh 24 h after the last antigen challenge. However, these animals did not show an increase in smooth muscle cell (SMC) number in the left main bronchus, suggesting that short-lived inflammatory mechanisms caused the acute AHR. In contrast, 7 days after the last aerosol challenge, there was a modest increase in SMC number, but no AHR to ACh. Addition of FCS to the chronic OA challenge protocol had no effect on the degree of inflammation but resulted in a marked increase in both SMC number and a persistent (7-day) AHR. These results raise the possibility that increases in airway SMC number rather than, or in addition to, chronic inflammation contribute to the persistent AHR detected in this model.
PubMed ID
12381772 View in PubMed
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Bronchial hyperresponsiveness, epithelial damage, and airway eosinophilia after single and repeated allergen exposure in a rat model of anhydride-induced asthma.

https://arctichealth.org/en/permalink/ahliterature15788
Source
Allergy. 1997 Jul;52(7):739-46
Publication Type
Article
Date
Jul-1997
Author
Z H Cui
M. Sjöstrand
T. Pullerits
P. Andius
B E Skoogh
J. Lötvall
Author Affiliation
Department of Clinical Pharmacology, Göteborg University, Sweden.
Source
Allergy. 1997 Jul;52(7):739-46
Date
Jul-1997
Language
English
Publication Type
Article
Keywords
Animals
Bronchi - immunology - pathology
Bronchial Hyperreactivity - immunology - pathology
Bronchial Provocation Tests
Eosinophilia - immunology
Epithelium - pathology
Humans
Immunoglobulin E - analysis
Immunoglobulin G - analysis
Male
Phthalic Anhydrides - administration & dosage - immunology
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Respiratory Hypersensitivity - immunology - pathology
Vaccination
Abstract
Bronchial hyperresponsiveness (BHR) and damage of the epithelium, as well as eosinophilia in the airway wall, induced by trimellitic anhydride (TMA) in sensitized brown Norway rats were studied. Rats were challenged once or seven times with aerosol of TMA conjugated to rat serum albumin (TMA-RSA) 3 weeks after intradermal TMA sensitization. Airway responsiveness (-log PC300 of acetylcholine i.v.) was measured 24 h after allergen challenge. Epithelial lesion and eosinophil infiltration in the airway walls were quantified under light microscopy, and TMA-specific IgE and IgG in serum were evaluated with ELISA. High levels of TMA-specific IgE and IgG were found in all rats in the sensitized groups compared to nonsensitized groups (P
PubMed ID
9265989 View in PubMed
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CD4+ T cells can induce airway hyperresponsiveness to allergen challenge in the brown norway rat.

https://arctichealth.org/en/permalink/ahliterature57554
Source
Am J Respir Crit Care Med. 1998 Dec;158(6):1863-70
Publication Type
Article
Date
Dec-1998
Author
H. Mishima
M. Hojo
A. Watanabe
Q A Hamid
J G Martin
Author Affiliation
Meakins-Christie Laboratories, Royal Victoria Hospital, McGill University, and the Respiratory Health Network of Centres of Excellence, Montreal, Quebec, Canada.
Source
Am J Respir Crit Care Med. 1998 Dec;158(6):1863-70
Date
Dec-1998
Language
English
Publication Type
Article
Keywords
Aerosols
Allergens - immunology
Animals
Bronchial Hyperreactivity - immunology
Bronchial Provocation Tests
Bronchoalveolar Lavage Fluid - chemistry - immunology
Bronchoconstrictor Agents - diagnostic use
CD4-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - immunology
Cattle
Comparative Study
Eosinophilia - immunology
Gene Expression Regulation
Immunization
Immunoglobulin E - immunology
In Situ Hybridization
Interferon Type II - genetics - immunology
Interleukin-5 - genetics - immunology
Male
Methacholine Chloride - diagnostic use
Ovalbumin - immunology
Proteins - analysis
RNA, Messenger - genetics
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Serum Albumin, Bovine - immunology
Time Factors
Abstract
Airway hyperresponsiveness to inhalational challenge with methacholine (MCh) develops by 32 h after allergen challenge of actively sensitized BN rats. To test the hypothesis that CD4+ T cells mediate allergen-induced hyperresponsiveness independent of IgE-mediated mechanisms, we administered CD4+ T cells, CD8+ T cells, and a mixture of CD4+ and CD8+ T cells (total T cells) isolated from the cervical lymph nodes of rats sensitized with ovalbumin (OA) to naive BN rats that underwent aerosol challenge with either OA or bovine serum albumin (BSA) 2 d later. Responsiveness to MCh was measured 2 d before transfer of T cells and 32 h after challenge with OA or BSA. Airway responsiveness increased significantly in recipients of CD4+ T cells after OA challenge, but not in any other of the treatment groups. Analysis of bronchoalveolar lavage (BAL) cells for major basic protein expression by immunostaining showed eosinophilia in OA-challenged CD4+ and total T-cell recipients. Cells retrieved by bronchoalveolar lavage showed increased expression of IL-5 mRNA (in situ hybridization) in CD4+ T cell recipients after OA challenge compared with other groups. Interferon-gamma mRNA was expressed to the greatest extent in CD8+ recipients, but it was elevated in both OA- and BSA-challenged animals. We conclude that CD4+ T cells can induce airway hyperresponsiveness after inhalational challenge with allergen and this is associated with IL-5 production and eosinophilia. CD8+ T cells may have a negative regulatory effect on responsiveness, possibly mediated by interferon-gamma.
PubMed ID
9847279 View in PubMed
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Childhood farm environment and asthma and sensitization in young adulthood.

https://arctichealth.org/en/permalink/ahliterature187520
Source
Allergy. 2002 Dec;57(12):1130-5
Publication Type
Article
Date
Dec-2002
Author
M. Kilpeläinen
E O Terho
H. Helenius
M. Koskenvuo
Author Affiliation
Department of Pulmonary Diseases and Clinical Allergology, University of Turku, Finland.
Source
Allergy. 2002 Dec;57(12):1130-5
Date
Dec-2002
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Animals
Animals, Domestic - immunology
Antibody Specificity - immunology
Asthma - etiology - physiopathology
Bronchial Hyperreactivity - immunology - physiopathology
Bronchial Provocation Tests
Bronchoconstrictor Agents - adverse effects - diagnostic use
Environmental Exposure - adverse effects
Female
Finland
Forced Expiratory Volume - drug effects - physiology
Humans
Immunization
Immunoglobulin E - blood - immunology
Male
Methacholine Chloride - adverse effects - diagnostic use
Questionnaires
Radioallergosorbent Test
Respiratory Function Tests
School Health Services
Severity of Illness Index
Skin Tests
Abstract
Farm environment in childhood may protect against sensitization, allergic rhinitis, and asthma.
Subjects were obtained from 10 667 Finnish first-year university students who responded to a questionnaire survey on IgE-mediated diseases. Two random samples were selected from 1631 respondents in Turku: subjects with asthma or wheezing, and subjects without asthmatic symptoms. A total of 296 subjects (72%) participated. Skin prick tests (SPT), measurements of IgE-antibodies, methacholine challenge, and bronchodilation tests were performed. Weighted occurrence of current asthma and sensitization among students from "childhood farm" and "childhood nonfarm" environments were analyzed.
Current asthma was found in 3.1% of subjects with childhood farm environment, and in 12.4% with nonfarm environment (odds ratio (OR) 0.22; 95% confidence interval (CI) 0.07-0.70). There were fewer positive SPT to birch (8.3 vs. 24.2%, OR 0.28, 95% CI 0.07-1.15) and timothy pollen (12.6 vs. 30.3%, OR 0.33, 95% CI 0.09-1.20) among subjects with childhood farm environment, but more sensitization to house-dust mite (22.0 vs. 4.9%, OR 5.43, 95% CI 1.60-18.46). Sensitization to cat (RAST class >/= 3) was less common in subjects with farm compared to nonfarm environments in childhood (1.5 vs. 13.1%; OR 0.10, 95% CI 0.02-0.47).
Farm environment in childhood protects against adult asthma and sensitization-especially to cat-the most important asthma related allergen. In contrast, sensitization to house-dust mite was more common in farming subjects.
PubMed ID
12464040 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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23 records – page 1 of 3.