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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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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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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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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 CD8+ T-cell depletion on bronchial hyper-responsiveness and inflammation in sensitized and allergen-exposed Brown-Norway rats.

https://arctichealth.org/en/permalink/ahliterature15670
Source
Immunology. 1999 Mar;96(3):416-23
Publication Type
Article
Date
Mar-1999
Author
T J Huang
P A MacAry
D M Kemeny
K F Chung
Author Affiliation
Thoracic Medicine, Chang Gung Memorial Hospital, Keelung Branch, Taiwan, China; Thoracic Medicine, National Heart & Lung Institute, Imperial College School of Medicine, London, UK.
Source
Immunology. 1999 Mar;96(3):416-23
Date
Mar-1999
Language
English
Publication Type
Article
Keywords
Acetylcholine - immunology
Allergens - immunology
Animals
Antibodies, Monoclonal - immunology
Asthma - immunology - physiopathology
Blotting, Southern
Bronchial Hyperreactivity - immunology
Bronchoalveolar Lavage Fluid - immunology
CD8-Positive T-Lymphocytes - immunology
Cytokines - biosynthesis
Immunoenzyme Techniques
Lung - immunology
Lymphocyte Count
Male
Mice
Ovalbumin - immunology
Rats
Rats, Inbred BN
Reverse Transcriptase Polymerase Chain Reaction
Vasodilator Agents - immunology
Abstract
We examined the role of CD8+ T cells in a Brown-Norway rat model of asthma, using a monoclonal antibody to deplete CD8+ T cells. Ovalbumin (OA)-sensitized animals were given anti-CD8 antibody (0.5 mg/rat) intravenously 1 week prior to exposure to 1% OA aerosol and were studied 18-24 hr after aerosol exposure. Following administration of anti-CD8 antibody, CD8+ cells were reduced to
PubMed ID
10233723 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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Effect of interleukin-1 beta on airway hyperresponsiveness and inflammation in sensitized and nonsensitized Brown-Norway rats.

https://arctichealth.org/en/permalink/ahliterature57706
Source
J Allergy Clin Immunol. 1994 Feb;93(2):464-9
Publication Type
Article
Date
Feb-1994
Author
H. Tsukagoshi
T. Sakamoto
W. Xu
P J Barnes
K F Chung
Author Affiliation
Department of Thoracic Medicine, National Heart and Lung Institute, Royal Brompton Hospital, London, England.
Source
J Allergy Clin Immunol. 1994 Feb;93(2):464-9
Date
Feb-1994
Language
English
Publication Type
Article
Keywords
Acetylcholine - pharmacology
Airway Resistance - drug effects - physiology
Animals
Bradykinin - pharmacology
Bronchial Hyperreactivity - etiology - pathology - physiopathology
Bronchoalveolar Lavage Fluid - cytology
Immunization
Inflammation - etiology - physiopathology
Interleukin-1 - pharmacology
Male
Ovalbumin - immunology
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Time Factors
Abstract
Airway responsiveness (AR) to inhaled acetylcholine and bradykinin and inflammatory cell recruitment in bronchoalveolar lavage fluid (BALF) were studied in inbred male Brown-Norway rats actively sensitized to ovalbumin and later given 500 U interleukin-1 beta (IL-1 beta) intratracheally. We examined animals 14 to 21 days after initial sensitization at 18 to 24 hours after the intratracheal administration of IL-1 beta. We evaluated AR to acetylcholine as -log PC200, which is -log10 transformation of provocative concentration of acetylcholine producing 200% increase in lung resistance, and to bradykinin as percent increase in lung resistance. BALF was examined as an index of inflammatory changes within the lung. Although there was no significant difference in baseline lung resistance, nonsensitized and sensitized animals that were given IL-1 beta demonstrated a significant increase of AR to bradykinin at 18 to 24 hours and a significant increase of neutrophil counts in BALF, which was already observed by 4 to 6 hours. There was a significant correlation between AR to bradykinin and neutrophil counts in BALF in all animals (r = 0.644; p
PubMed ID
8120273 View in PubMed
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Involvement of cysteinyl leukotrienes in airway smooth muscle cell DNA synthesis after repeated allergen exposure in sensitized Brown Norway rats.

https://arctichealth.org/en/permalink/ahliterature15646
Source
Br J Pharmacol. 1999 Jul;127(5):1151-8
Publication Type
Article
Date
Jul-1999
Author
M. Salmon
D A Walsh
T J Huang
P J Barnes
T B Leonard
D W Hay
K F Chung
Author Affiliation
Thoracic Medicine, Imperial College School of Medicine at the National Heart and Lung Institute, London, UK.
Source
Br J Pharmacol. 1999 Jul;127(5):1151-8
Date
Jul-1999
Language
English
Publication Type
Article
Keywords
Acetylcholine - pharmacology
Allergens - immunology
Animals
Arachidonate 5-Lipoxygenase - physiology
Bronchi - drug effects - metabolism
Cell Count
Cysteine - physiology
DNA - biosynthesis
Eosinophils - physiology
Leukotrienes - physiology
Male
Muscle, Smooth - metabolism
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Abstract
Airway smooth muscle thickening is a characteristic feature of airway wall remodelling in chronic asthma. We have investigated the role of the leukotrienes in airway smooth muscle (ASM) and epithelial cell DNA synthesis and ASM thickening following repeated allergen exposure in Brown Norway rats sensitized to ovalbumin. There was a 3 fold increase in ASM cell DNA synthesis, as measured by percentage bromodeoxyuridine (BrdU) incorporation, in repeatedly ovalbumin-exposed (4.1%, 3.6-4.6; mean, 95% c.i.) compared to chronically saline-exposed rats (1.3%, 0.6-2.1; P
PubMed ID
10455261 View in PubMed
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Mechanisms of impaired beta-adrenoceptor-induced airway relaxation by interleukin-1beta in vivo in the rat.

https://arctichealth.org/en/permalink/ahliterature11157
Source
J Clin Invest. 1996 Oct 15;98(8):1780-7
Publication Type
Article
Date
Oct-15-1996
Author
H. Koto
J C Mak
E B Haddad
W B Xu
M. Salmon
P J Barnes
K F Chung
Author Affiliation
Thoracic Medicine, National Heart and Lung Institute, Imperial College of Science, Technology and Medicine, London, United Kingdom.
Source
J Clin Invest. 1996 Oct 15;98(8):1780-7
Date
Oct-15-1996
Language
English
Publication Type
Article
Keywords
Animals
Autoradiography
Bronchi - drug effects - physiology
Cyclic AMP - metabolism
Forskolin - pharmacology
GTP-Binding Proteins - analysis
Interleukin-1 - pharmacology
Isoproterenol - pharmacology
Muscle Relaxation - drug effects
RNA, Messenger - analysis
Rats
Rats, Inbred BN
Receptors, Adrenergic, beta - analysis - genetics - physiology
Research Support, Non-U.S. Gov't
Trachea - drug effects - physiology
Abstract
We studied the in vivo mechanism of beta-adrenergic receptor (beta-AR) hyporesponsiveness induced by intratracheal instillation of interleukin-1beta (IL-1beta, 500 U) in Brown-Norway rats. Tracheal and bronchial smooth muscle responses were measured under isometric conditions ex vivo. Contractile responses to electrical field stimulation and to carbachol were not altered, but maximal relaxation induced by isoproterenol (10(-6)-10(-5) M) was significantly reduced 24 h after IL-1beta treatment in tracheal tissues and to a lesser extent, in the main bronchi. Radioligand binding using [125I]iodocyanopindolol revealed a 32+/-7% reduction in beta-ARs in lung tissues from IL-1beta-treated rats, without any significant changes in beta2-AR mRNA level measured by Northern blot analysis. Autoradiographic studies also showed significant reduction in beta2-AR in the airways. Isoproterenol-stimulated cyclic AMP accumulation was reduced by IL-1beta at 24 h in trachea and lung tissues. Pertussis toxin reversed this hyporesponsiveness to isoproterenol but not to forskolin in lung tissues. Western blot analysis revealed an IL-1beta-induced increase in Gi(alpha) protein expression. Thus, IL-1beta induces an attenuation of beta-AR-induced airway relaxation through mechanisms involving a reduction in beta-ARs, an increase in Gi(alpha) subunit, and a defect in adenylyl cyclase activity.
PubMed ID
8878428 View in PubMed
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14 records – page 1 of 2.