Skip header and navigation

Refine By

5 records – page 1 of 1.

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
Less detail

CD26 (dipeptidyl-peptidase IV)-dependent recruitment of T cells in a rat asthma model.

https://arctichealth.org/en/permalink/ahliterature15108
Source
Clin Exp Immunol. 2005 Jan;139(1):17-24
Publication Type
Article
Date
Jan-2005
Author
C. Kruschinski
T. Skripuletz
S. Bedoui
T. Tschernig
R. Pabst
C. Nassenstein
A. Braun
S. von Hörsten
Author Affiliation
Department of Functional and Applied Anatomy, Medical School of Hannover, Hannover, Germany.
Source
Clin Exp Immunol. 2005 Jan;139(1):17-24
Date
Jan-2005
Language
English
Publication Type
Article
Keywords
Animals
Antigens, CD26 - immunology
Asthma - blood - immunology
Bronchoalveolar Lavage Fluid - immunology
CD4 Lymphocyte Count
CD4-Positive T-Lymphocytes - immunology
Comparative Study
Disease Models, Animal
Eosinophils - immunology
Immunoglobulin E - blood
Lymphocyte Count
Lymphocytes - immunology
Ovalbumin - immunology
Rats
Rats, Inbred BN
Rats, Inbred F344
Rats, Inbred Lew
Receptors, Antigen, T-Cell - immunology
Research Support, Non-U.S. Gov't
T-Lymphocytes - immunology
Abstract
CD26 truncates several chemokines as well as neuropeptides and influences immune responses via modulation of cell adhesion and T cell activation, suggesting an involvement of CD26 in asthmatic and airway inflammation. Therefore, Fischer 344 (F344), Brown Norway (BN) and Lewis (LEW) rat strains, which differ in their CD26-like enzymatic activity, were compared using an asthma model. Additionally, two CD26-deficient mutant F344 rat substrains were included and compared to the wild-type F344 substrain. Immunization was performed twice with ovalbumin (OVA), and 2 weeks later the rats were challenged with OVA intratracheally Flow cytometry (FACS) analysis of different leucocyte subsets as well as enzyme-linked immunosorbent assay (ELISA) for IgE levels in the blood and bronchoalveolar lavage (BAL) were performed 24 h after challenge. LEW rats with the lowest CD26 activity among the rat strains investigated here displayed significantly reduced CD4+ T cell numbers in the BAL compared to wild-type F344 and BN rats. Moreover, in asthma, the ratio of CD26+ to CD26- T cell receptor (TCR)-positive cells increased significantly in F344 and LEW but not BN rats. Most intriguingly, in both CD26-deficient F344 rat substrains the number of CD4+ T lymphocytes was markedly reduced compared to wild-type F344. The decrease in T cell recruitment observed in the CD26-deficient rats was associated with significantly reduced OVA-specific IgE-titres. This is the first report to show a remarkably reduced T cell recruitment in rat strains that either lack or exhibit reduced CD26-like enzymatic activity, suggesting a role for CD26 in the pathogenesis of asthma via T cell-dependent processes such as antibody production.
Notes
Erratum In: Clin Exp Immunol. 2005 Apr;140(1):192
PubMed ID
15606609 View in PubMed
Less detail

Effect of an inhibitor of Jun N-terminal protein kinase, SP600125, in single allergen challenge in sensitized rats.

https://arctichealth.org/en/permalink/ahliterature15159
Source
Immunology. 2004 Jul;112(3):446-53
Publication Type
Article
Date
Jul-2004
Author
Paul R Eynott
Li Xu
Brydon L Bennett
Alistair Noble
Sum-Yee Leung
Puneeta Nath
David A Groneberg
Ian M Adcock
K Fan Chung
Author Affiliation
Thoracic Medicine, National Heart and Lung Institute, Imperial College School of Medicine, London, UK.
Source
Immunology. 2004 Jul;112(3):446-53
Date
Jul-2004
Language
English
Publication Type
Article
Keywords
Allergens - pharmacology
Animals
Anthracenes - pharmacology
Asthma - immunology
Bronchoalveolar Lavage Fluid - immunology
Cell Count
Cytokines - immunology
Enzyme Activation
Eosinophils - immunology
JNK Mitogen-Activated Protein Kinases
Leukocyte Count
Leukocytes, Mononuclear - immunology
Lung - enzymology - immunology
MAP Kinase Kinase 4
Macrophages - immunology
Male
Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors - metabolism
Mitogen-Activated Protein Kinases - metabolism
Models, Animal
Neutrophils - immunology
Ovalbumin
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
p38 Mitogen-Activated Protein Kinases
Abstract
Jun N-terminal kinase (JNK) has been implicated in the pathogenesis of inflammatory diseases including asthma. We examined the effect of SP600125 (anthra [1,9-cd] pyrazol-6 (2H)-one), a novel inhibitor of JNK in a model of asthma. Brown-Norway rats were sensitized to ovalbumin and treated with SP600125 intraperitoneally (90 mg/kg in total). SP600125 inhibited allergen-induced, increased activity of phosphorylated c-jun but not of phosphorylated-MAPKAPK2, indicative of activation of p38 MAPK, in the lung. SP600125 inhibited macrophage (P
PubMed ID
15196213 View in PubMed
Less detail

Pulmonary function changes and increased Th-2 cytokine expression and nuclear factor kB activation in the lung after sensitization and allergen challenge in brown Norway rats.

https://arctichealth.org/en/permalink/ahliterature15559
Source
Immunol Lett. 2000 Jul 3;73(1):57-64
Publication Type
Article
Date
Jul-3-2000
Author
C C Lin
C Y Lin
H Y Ma
Author Affiliation
Chest Division and Department of Medical Research, Mackay Memorial Hospital, 92, Sec 2, Chung Shan North Road, Taipei, Taiwan, ROC.
Source
Immunol Lett. 2000 Jul 3;73(1):57-64
Date
Jul-3-2000
Language
English
Publication Type
Article
Keywords
Allergens - immunology
Animals
Asthma - immunology - physiopathology
Bronchial Hyperreactivity - immunology - physiopathology
Bronchial Provocation Tests
Bronchoalveolar Lavage Fluid - immunology
Cytokines - genetics - metabolism
Eosinophils - immunology
Lung - immunology - pathology - physiopathology
Male
Maximal Expiratory Flow Rate
NF-kappa B - immunology - metabolism
Ovalbumin - immunology
RNA, Messenger - biosynthesis
Rats
Research Support, Non-U.S. Gov't
Th2 Cells - metabolism
Abstract
BACKGROUND: Our purpose was to evaluate the expression of Th-1 and Th-2 related cytokine mRNA and nuclear factor (NF) kB in the lung tissue of ovalbumin (OA) sensitized brown Norway rats (BNR). We also evaluated the correlation between bronchial hyperreactivity (BHR) and eosinophils with cytokine mRNA expression. METHODS: Eight BNR (weight range 250-350 g) were sensitized by inhaled OA (group I) with a 1-week interval between and then provoked with OA 1 week later. Pulmonary function tests (PFT) were performed at baseline and 24 h after acetylcholine challenge. Eight weight-matched normal BNR served as controls (group II). All animals were anesthetized, paralyzed with gallamine, and ventilated via tracheostomy. They were given varying doses of acetylcholine (25, 50, 75, 100 microg/kg) injected through a jugular venous catheter. Five seconds after acetylcholine injections, PFTs were performed, including a maximal forced expiratory maneuver (MFEM), airway opening pressure (P(ao)) at tidal breathing and total dynamic lung compliance (C(dyn)). Bronchoalveolar lavage (BAL) was then performed with 20 ml normal saline divided into two doses. Thereafter, the lungs were removed and examined histologically. Total RNA was extracted from lung tissue samples and reverse-transcriptase polymerase chain reaction was performed using primers for mRNA of IL-4, IL-5, IL-10, interferon-gamma (IFNr) and beta-actine. RESULTS: Group I OA treated rats had typical airway obstruction on PFTs and airway inflammation on histological examination. Ratios of IL-4, IL-5, IL-10 and inducible nitric oxide synthase (iNOS) mRNA levels to beta-actine as measured by densitometry were significantly lower in controls than in OA-sensitized rats. The IFNr mRNA to beta-actin ratio was significantly reduced in OA-sensitized rats. Group I demonstrated a band shift when compared with group II in electromobility shift assay (EMSA) for NF-kB indicating increased activation of this transcription factor. CONCLUSION: Th-2 related cytokine mRNA was increased but Th-1 related cytokine mRNA was decreased in OA-sensitized BNR. An increased level of Th-2 related cytokine mRNA correlated with decreased airflow and inflammatory changes. These results demonstrate the value of the BNR model for studying allergic asthma at the molecular level.
PubMed ID
10963812 View in PubMed
Less detail

Resolution of allergic airways inflammation but persistence of airway smooth muscle proliferation after repeated allergen exposures.

https://arctichealth.org/en/permalink/ahliterature15187
Source
Clin Exp Allergy. 2004 Feb;34(2):213-20
Publication Type
Article
Date
Feb-2004
Author
S-Y Leung
P. Eynott
A. Noble
P. Nath
K F Chung
Author Affiliation
Thoracic Medicine, National Heart and Lung Institute, Imperial College, London, UK.
Source
Clin Exp Allergy. 2004 Feb;34(2):213-20
Date
Feb-2004
Language
English
Publication Type
Article
Keywords
Allergens - administration & dosage
Animals
Antigens, CD2 - analysis
Asthma - immunology
Bronchi - immunology - pathology
Bronchial Hyperreactivity - immunology - pathology
Bronchoalveolar Lavage Fluid - immunology
Cell Division
Eosinophils - immunology
Immunoglobulin E - blood
Leukocytes - immunology
Male
Muscle, Smooth - immunology - pathology
Ovalbumin
Rats
Rats, Inbred BN
T-Lymphocytes - immunology
Time Factors
Abstract
BACKGROUND: Chronic inflammation in asthmatic airways can lead to characteristic airway smooth muscle (ASM) thickening and pathological changes within the airway wall. OBJECTIVE: We investigated the long-term effects of repeated allergen exposure. METHODS: Brown-Norway (BN) rats sensitized to ovalbumin (OVA) were exposed to OVA or saline aerosol every third day on six occasions and studied 24 h, 7 days and 35 days after the final exposure. We measured airway inflammation, ASM cell proliferation (by incorporation of bromodeoxyuridine; BrdU) and bronchial responsiveness to acetylcholine. RESULTS: At 24 h, in OVA-exposed rats, we detected elevated OVA-specific serum IgE, increased numbers of macrophages, eosinophils, lymphocytes and neutrophils in the bronchoalveolar lavage (BAL) fluid and increased numbers of MBP+ (major basic protein) eosinophils and CD2+ T cells within the bronchial submucosa. This coincided with increased numbers of ASM cells expressing BrdU and with bronchial hyper-responsiveness (BHR). At 7 days, BHR was detected in OVA-exposed rats, coincident with increased numbers of macrophages and lymphocytes in BAL fluid together with increased numbers of CD2+ T cells within the bronchial submucosa. This coincided with increased numbers of ASM cells expressing BrdU. By day 35, the number of ASM cells expressing BrdU remained elevated in the absence of cellular infiltration and BHR. CONCLUSION: Repeated OVA-challenge results in persistent ASM cell proliferation in the absence of bronchial inflammation and BHR, which lasts for at least 1 week following cessation of exposure.
PubMed ID
14987300 View in PubMed
Less detail