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Adjuvant effect of respiratory irritation on pulmonary allergic sensitization: time and site dependency.

https://arctichealth.org/en/permalink/ahliterature15794
Source
Toxicol Appl Pharmacol. 1997 Jun;144(2):356-62
Publication Type
Article
Date
Jun-1997
Author
P D Siegel
N H Al-Humadi
E R Nelson
D M Lewis
A F Hubbs
Author Affiliation
Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505, USA.
Source
Toxicol Appl Pharmacol. 1997 Jun;144(2):356-62
Date
Jun-1997
Language
English
Publication Type
Article
Keywords
Adjuvants, Immunologic - toxicity
Ammonia - toxicity
Animals
Asthma - chemically induced - immunology
Bronchoalveolar Lavage Fluid - cytology
Immunoglobulins - blood - drug effects
Irritants - toxicity
Lung - drug effects - immunology - pathology
Male
Nitrogen Dioxide - toxicity
Ovalbumin - immunology
Rats
Time Factors
Abstract
It has been suggested that airway irritation, by acting as an adjuvant, as well as producing damage, may be an important factor related to asthma. The present study examined the window of time following acute upper and lower airway irritant exposure to determine the period of increased risk of immunological sensitization. Brown Norway rats were exposed to 87 ppm NO2 or 1000 ppm NH3 for 1 hr. A 30-min ovalbumin (OVA) exposure of 18.14 microg/liter air was given at various times based upon the time course of irritant associated inflammatory response (either immediately prior to or 1 or 7 days after the irritant exposure). OVA-only, NO2-only or NH3-only controls, and saline controls were also studied. Weekly booster exposures of OVA (or saline) were given. Circulating OVA-specific IgE, IgA, and IgG levels were quantified periodically during the 6 weeks of the study. Bronchoalveolar lavage (BAL) was also performed to examine the inflammatory response to allergic and irritant challenge. Significant increases in OVA-specific IgE, IgG, and IgA antibody titers were seen in rats given the sensitizing OVA exposure within 1 day of the NO2, but not NH3 exposures. Enhancement of cellular infiltrate in BAL was noted in groups given the sensitizing OVA exposure within 1 day of the NO2 or NH3. It is concluded that the inflammatory and immunological response to antigen exposure can be modified by the site of respiratory tract irritation and the relative times of irritant and antigen exposure.
PubMed ID
9194420 View in PubMed
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Adoptively transferred late allergic airway responses are associated with Th2-type cytokines in the rat.

https://arctichealth.org/en/permalink/ahliterature57629
Source
Am J Respir Cell Mol Biol. 1997 Jan;16(1):69-74
Publication Type
Article
Date
Jan-1997
Author
A. Watanabe
H. Mishima
T C Kotsimbos
M. Hojo
P M Renzi
J G Martin
Q A Hamid
Author Affiliation
Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada.
Source
Am J Respir Cell Mol Biol. 1997 Jan;16(1):69-74
Date
Jan-1997
Language
English
Publication Type
Article
Keywords
Adoptive Transfer
Airway Resistance
Animals
Bronchoalveolar Lavage Fluid - cytology - immunology
CD4-Positive T-Lymphocytes - immunology - transplantation
CD8-Positive T-Lymphocytes - immunology - transplantation
Interferon Type II - biosynthesis
Interleukin-2 - biosynthesis
Interleukin-4 - biosynthesis
Interleukin-5 - biosynthesis
Interleukins - biosynthesis
Ovalbumin - immunology
Rats
Research Support, Non-U.S. Gov't
Respiratory Hypersensitivity - immunology
Th2 Cells - immunology
Abstract
Late allergic airway responses can be transferred by CD4+ T cells in the rat. To investigate the role of T-cell cytokines in these responses, we examined the expression of mRNA for Th2 (interleukin [IL]-4 and IL-5) and Th1 (IL-2 and interferon gamma [INF-gamma])-type cytokines in Brown Norway rats that were administered either antigen-primed W3/25(CD4)+ or OX8(CD8)+ T cells. Donors were actively sensitized by subcutaneous injection of ovalbumin (OVA) in the neck and T cells were obtained from the cervical lymph nodes by immunomagnetic cell sorting for administration to unsensitized rats. Control rats received bovine serum albumin (BSA)-primed CD4+ and CD8+ T cells. Two days later, recipient rats were challenged with aerosolized OVA, and bronchoalveolar lavage (BAL) was performed 8 h after challenge. BAL cells expressing mRNA for IL-2, IL-4, IL-5, and INF-gamma were analyzed using the technique of in situ hybridization. Recipients of OVA-primed CD4+ T cells had an increase in the fraction of BAL cells expressing mRNA for IL-4 and IL-5 compared with BSA-primed CD4+ or OVA-primed CD8+ cells (P
PubMed ID
8998081 View in PubMed
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Adoptively transferred late allergic response is inhibited by IL-4, but not IL-5, antisense oligonucleotide.

https://arctichealth.org/en/permalink/ahliterature15653
Source
J Allergy Clin Immunol. 1999 Jul;104(1):205-14
Publication Type
Article
Date
Jul-1999
Author
S. Molet
D. Ramos-Barbón
J G Martin
Q. Hamid
Author Affiliation
Meakins-Christie Laboratories, McGill University, Montréal, Quebec, Canada.
Source
J Allergy Clin Immunol. 1999 Jul;104(1):205-14
Date
Jul-1999
Language
English
Publication Type
Article
Keywords
Adoptive Transfer
Animals
Asthma - immunology - prevention & control
Bronchoalveolar Lavage Fluid - chemistry - cytology
CD4-Positive T-Lymphocytes - drug effects
Cell Survival
Cells, Cultured
Cytokines - immunology
Disease Models, Animal
Immunohistochemistry
Interleukin-4 - immunology - therapeutic use
Interleukin-5 - immunology - therapeutic use
Male
Oligonucleotides, Antisense - therapeutic use
Ovalbumin - pharmacology
Pulmonary Eosinophilia - metabolism
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Th2 Cells - immunology
Abstract
BACKGROUND: We have shown previously that the late airways response (LAR) can be transferred by ovalbumin-primed CD4(+) T lymphocytes in Brown Norway rats. This response is associated with an increase of eosinophils and high expression of TH2 cytokines (IL-4 and IL-5) in bronchoalveolar lavage (BAL) fluid. OBJECTIVE: In this study we hypothesized that the inhibition of IL-4 or IL-5 production in the CD4(+) cells transferred to a naive animal could decrease the LAR and prevent airway eosinophilia in response to antigen challenge. METHODS: CD4(+) cells, purified from the cervical lymph nodes of ovalbumin-sensitized rats, were maintained in culture for 6 hours with medium alone or with 10 microgram/mL IL-4 antisense (AS), IL-5 AS, or control AS oligodeoxynucleotide. Then the cells were administrated intraperitoneally to naive rats, which were challenged 2 days later by a 5% ovalbumin aerosol. The lung resistance was measured for 8 hours, and then BAL was performed. Cytospin preparations from BAL cells were assessed for the presence of eosinophils by immunocytochemistry for major basic protein and for IL-4, IL-5, and IFN-gamma expression. RESULTS: In rats injected with IL-4 AS-treated T cells, LAR, eosinophils, and IL-4 and IL-5 expression were significantly decreased compared with the other groups. Only IL-5 expression in BAL fluid was slightly decreased consequent to the transfer of IL-5 AS-treated T cells. CONCLUSION: This study demonstrates that, in the CD4(+) T cell-driven LAR, the early production of IL-4, but not IL-5, by the transferred CD4(+) cells is essential for the development of the LAR.
Notes
Erratum In: J Allergy Clin Immunol 1999 Dec;104(6):1188
PubMed ID
10400863 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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Adoptive transfer of alveolar macrophages abrogates bronchial hyperresponsiveness.

https://arctichealth.org/en/permalink/ahliterature15196
Source
Am J Respir Cell Mol Biol. 2004 Jul;31(1):22-7
Publication Type
Article
Date
Jul-2004
Author
Eric Careau
Elyse Y Bissonnette
Author Affiliation
Centre de Recherche, Hôpital Laval, Institut universitaire de Cardiologie et de Pneumologie de l'Université Laval, Québec, Canada. eric.careau@crhl.ulaval.ca
Source
Am J Respir Cell Mol Biol. 2004 Jul;31(1):22-7
Date
Jul-2004
Language
English
Publication Type
Article
Keywords
Adoptive Transfer
Animals
Asthma - physiopathology
Bronchi - drug effects - immunology - physiopathology
Bronchial Hyperreactivity - genetics - physiopathology - therapy
Bronchial Provocation Tests
Clodronic Acid
Disease Models, Animal
Dose-Response Relationship, Drug
Drug Resistance - physiology
Genetic Predisposition to Disease - genetics
Immunoglobulin E - blood
Immunoglobulin G - blood
Liposomes
Macrophages, Alveolar - drug effects - immunology - transplantation
Male
Methacholine Chloride - pharmacology
Ovalbumin - immunology
Rats
Rats, Sprague-Dawley
Reaction Time - drug effects - physiology
Research Support, Non-U.S. Gov't
Abstract
Increasing evidence suggests that alveolar macrophages (AM) are involved in asthma pathogenesis. To better understand the role that these cells play, we investigated the capacity of AM from allergy-resistant rat, Sprague Dawley (SD), to modulate airway hyperresponsiveness of allergy-susceptible rat, Brown Norway (BN). AM of ovalbumin (OVA)-sensitized BN rats were eliminated by intratracheal instillation of liposomes containing clodronate. AM from OVA-sensitized SD rats were transferred into AM-depleted BN rats 24 h before allergen challenge. Airway responsiveness to methacholine was measured the following day. Instillation of liposomes containing clodronate in BN rats eliminated 85% AM after 3 d compared with saline liposomes. Methacholine concentration needed to increase lung resistance by 200% (EC200RL) was significantly lower in OVA-challenged BN rats (27.9 +/- 2.8 mg/ml) compared with SD rats (63.9 +/- 8.6 mg/ml). However, when AM from SD rats were transferred into AM-depleted BN rats, airway responsiveness (64.0 +/- 11.3 mg/ml) was reduced to the level of naïve rats (54.4 +/- 3.7 mg/ml) in a dose-dependent manner. Interestingly, transfer of AM from BN rats into SD rats did not modulate airway responsiveness. To our knowledge, this is the first direct evidence showing that AM may protect against the development of airway hyperresponsiveness.
Notes
Comment In: Am J Respir Cell Mol Biol. 2004 Jul;31(1):1-215208095
Comment In: Am J Respir Cell Mol Biol. 2004 Jul;31(1):3-715208096
PubMed ID
14962974 View in PubMed
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Ag-specific recognition, activation, and effector function of T cells in the conjunctiva with experimental immune-mediated blepharoconjunctivitis.

https://arctichealth.org/en/permalink/ahliterature50675
Source
Invest Ophthalmol Vis Sci. 2003 Oct;44(10):4366-74
Publication Type
Article
Date
Oct-2003
Author
Atsuki Fukushima
Akemi Ozaki
Kazuyo Fukata
Waka Ishida
Hisayuki Ueno
Author Affiliation
Department of Ophthalmology, Kochi Medical School, Nankoku City, Japan. fukusima@kochi-ms.ac.jp
Source
Invest Ophthalmol Vis Sci. 2003 Oct;44(10):4366-74
Date
Oct-2003
Language
English
Publication Type
Article
Keywords
Animals
Blepharitis - immunology
Blotting, Western
Chemokines - metabolism
Conjunctiva - immunology
Conjunctivitis - immunology
Cytokines - metabolism
Epitopes - immunology
Flow Cytometry
Fluoresceins
Immunoenzyme Techniques
Immunophenotyping
Lymphocyte Activation - physiology
Male
Mice
Mice, Inbred BALB C
Ovalbumin - immunology
Rats
Rats, Inbred BN
Receptors, Chemokine - metabolism
Research Support, Non-U.S. Gov't
Reverse Transcriptase Polymerase Chain Reaction
Succinimides
T-Lymphocytes - physiology
Abstract
PURPOSE. To investigate antigen (Ag) specificity, activation, and effector function of the Ag-specific T cells involved in the development of experimental immune-mediated blepharoconjunctivitis (EC), an experimental conjunctivitis. METHODS. EC was induced in Brown Norway rats by injection of ovalbumin (OVA)-specific T cells followed by OVA challenge with eye drops. Eyes, including the conjunctivas, were harvested at different time points after challenge. The dependence of EC onset on the challenging Ag was assessed by challenge with an irrelevant Ag or stimulatory OVA peptides. To show the infiltration of transferred T cells into the conjunctiva, T cells were labeled with 5-(and-6)-carboxyfluorescein diacetate succinimidyl ester (CFSE) before transfer. The activation of T cells in the conjunctiva was assessed by measuring phosphorylation of Lck-associated molecules by Western blot analysis. Conjunctivas were also examined by immunohistochemistry and used for reverse transcription-polymerase chain reaction to determine the phenotype of the infiltrating cells and cytokine, chemokine, and chemokine receptor expression. To investigate infiltration of non Ag-specific T cells into the conjunctiva, ragweed (RW)-primed lymphocytes were transferred into OVA-specific T-cell receptor transgenic (DO11.10) mice. The mice were then challenged with RW and the conjunctivas were harvested for immunohistochemistry to detect T cells derived from DO11.10 mice. RESULTS. EC was induced only when challenged with OVA protein or stimulatory OVA peptides, and CFSE-labeled transferred cells were found in the conjunctiva. Phosphorylation of Lck and an 85-kDa Lck-associated molecule were observed in the conjunctiva 6 hours after challenge. Many cytokines and chemokines began to be expressed at 6 hours, and individual expression patterns over time correlated well with the infiltration patterns of different inflammatory cells. In DO11.10 mice that received RW-primed lymphocytes, T cells derived from the recipient mice infiltrated the conjunctiva after RW challenge. CONCLUSIONS. Ag-specific T cells initiate EC by first infiltrating the conjunctiva, where they become activated by the specific Ag in the conjunctiva.
PubMed ID
14507881 View in PubMed
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Airway and tissue behavior during early response in sensitized rats: role of 5-HT and LTD4.

https://arctichealth.org/en/permalink/ahliterature15868
Source
J Appl Physiol. 1996 Feb;80(2):583-90
Publication Type
Article
Date
Feb-1996
Author
T. Nagase
M J Dallaire
M S Ludwig
Author Affiliation
Meakins-Christie Laboratories and Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada.
Source
J Appl Physiol. 1996 Feb;80(2):583-90
Date
Feb-1996
Language
English
Publication Type
Article
Keywords
Air Pressure
Airway Resistance - physiology
Animals
Basement Membrane - physiology
Constriction, Pathologic - physiopathology
Elasticity
Leukotriene D4 - antagonists & inhibitors - physiology
Lung - pathology
Ovalbumin - administration & dosage - immunology
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Respiratory Function Tests
Respiratory Hypersensitivity - pathology - physiopathology
Serotonin - physiology
Serotonin Antagonists - pharmacology
Abstract
We have recently demonstrated that tissue resistance increases during the early response (ER) to antigen challenge in sensitized Brown-Norway rats. The purpose of the present study was to investigate the role of the potential ER mediators 5-hydroxytryptamine (5-HT) and leukotriene D4 (LTD4) in the airway and tissue response. We sensitized the rats with ovalbumin (OA) and performed experiments on anesthetized, open-chested, mechanically ventilated [breathing frequency = 1 Hz, tidal volume = 12 ml/kg, positive end-expiratory pressure (PEEP) = 3 cmH2O] animals. We affixed alveolar capsules to the lungs to measure alveolar pressure and calculated the resistance of lung (RL), tissue (Rti), and airway (Raw). To assess the effects of LTD4 and 5-HT, we administered the antagonists methysergide (5-HT antagonist) and MK-571 (LTD4 antagonist) before challenge. To assess lung morphometry during the ER, the lungs of four animals from each group were frozen with liquid nitrogen (PEEP = 3 cmH2O). Airway constriction was assessed by measuring the ratio of the airway lumen to the ideally relaxed airway (Abm/A*bm). Tissue distortion was assessed by measuring the mean linear intercept between alveolar walls (Lm), an atelectasis index (ATI) derived by calculating the ratio of tissue to air space, and SD of the two (SD-Lm and SD-ATI). In all animals receiving OA but no antagonists, an ER was seen (RL, Rti, and Raw = 180.7 +/- 6.1, 155.4 +/- 8.2, and 223.1 +/- 14.0% of baseline, respectively). Methysergide significantly inhibited the ER (RL, Rti, and Raw = 117.0 +/- 5.9, 101.2 +/- 1.6, 133.7 +/- 10.2%, respectively), whereas MK-571 partially reduced the ER (RL, Rti, and Raw = 144.2 +/- 5.6, 132.9 +/- 5.7, and 155.5 +/- 9.2%, respectively). Abm/A*bm was significantly decreased, and SD-Lm and SD-ATI were significantly increased in animals receiving OA alone and in those receiving MK-571 before OA challenge. These data suggest that alterations in both airways and tissues contribute to the ER and that 5-HT and, to a lesser degree, LTD4 are important mediators of the ER in this rat model of extrinsic asthma.
PubMed ID
8929602 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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155 records – page 1 of 16.