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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
Less detail

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
Less detail

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
Less detail

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 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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Allergic rhinitis model with Brown Norway rat and evaluation of antiallergic drugs.

https://arctichealth.org/en/permalink/ahliterature57788
Source
J Pharmacobiodyn. 1990 Jul;13(7):414-20
Publication Type
Article
Date
Jul-1990
Author
N. Takahashi
Y. Aramaki
S. Tsuchiya
Author Affiliation
Tokyo College of Pharmacy, Japan.
Source
J Pharmacobiodyn. 1990 Jul;13(7):414-20
Date
Jul-1990
Language
English
Publication Type
Article
Keywords
Acetylglucosaminidase - secretion
Administration, Topical
Animals
Anti-Inflammatory Agents - pharmacology
Antigens - immunology
Biological Markers
Chlorpheniramine - pharmacology
Disease Models, Animal
Evans Blue - metabolism
Fluprednisolone - analogs & derivatives - pharmacology
Histamine Release - immunology
Immunization
Immunoglobulin E - biosynthesis
Male
Nasal Cavity - immunology
Nasal Mucosa - secretion
Ovalbumin - immunology
Rats
Rats, Inbred BN - blood - immunology
Rats, Inbred Strains
Rhinitis, Allergic, Perennial - chemically induced - drug therapy - immunology
Abstract
An animal disease model of allergic rhinitis was developed with Brown Norway (BN) rat, a high immunoglobulin E responder strain. BN rats were immunized with ovalbumin (OA) and made to suffer from allergic rhinitis. The severity of allergic rhinitis was assessed by determining the extent of the three kinds of markers, Evan's blue, histamine and N-acetyl-beta-D-glucosaminidase, released into the nasal perfusate following the OA challenge to the nasal cavity of OA-sensitized BN rats. This experimental system was appreciated by antiallergic drugs; chlorpheniramine maleate inhibited the release of Evan's blue and elevated that of histamine, but did not affect the N-acetyl-beta-D-glucosaminidase level. Halopredone acetate inhibited the releases of all the three markers. The estimation of the released markers using allergic rhinitis brought about in BN rats was found to be a useful experimental system for evaluating the effect of drugs on allergic rhinitis.
PubMed ID
1705288 View in PubMed
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Allergic sensitization and microbial load--a comparison between Finland and Russian Karelia.

https://arctichealth.org/en/permalink/ahliterature165130
Source
Clin Exp Immunol. 2007 Apr;148(1):47-52
Publication Type
Article
Date
Apr-2007
Author
T. Seiskari
A. Kondrashova
H. Viskari
M. Kaila
A-M Haapala
J. Aittoniemi
M. Virta
M. Hurme
R. Uibo
M. Knip
H. Hyöty
Author Affiliation
Department of Virology, University of Tampere, Finland. tapio.seiskari@uta.fi
Source
Clin Exp Immunol. 2007 Apr;148(1):47-52
Date
Apr-2007
Language
English
Publication Type
Article
Keywords
Adolescent
Allergens - immunology
Animals
Antibodies, Bacterial - blood
Antibodies, Protozoan - blood
Antibodies, Viral - blood
Bacteria - isolation & purification
Betula - immunology
Cats - immunology
Child
Enterovirus B, Human - immunology - isolation & purification
Female
Finland - epidemiology
Helicobacter pylori - immunology - isolation & purification
Hepatitis A virus - immunology - isolation & purification
Humans
Hypersensitivity - ethnology - immunology - microbiology
Immunoglobulin E - blood
Male
Ovalbumin - immunology
Pollen - immunology
Russia - epidemiology
Toxoplasma - immunology - isolation & purification
Viruses - isolation & purification
Abstract
Epidemiological data have indicated that some infections are associated with a low risk of allergic diseases, thus supporting the idea (hygiene hypothesis) that the microbial load is an important environmental factor conferring protection against the development of allergies. We set out to test the hygiene hypothesis in a unique epidemiological setting in two socio-economically and culturally markedly different, although genetically related, populations living in geographically adjacent areas. The study cohorts included 266 schoolchildren from the Karelian Republic in Russia and 266 schoolchildren from Finland. The levels of total IgE and allergen-specific IgE for birch, cat and egg albumen were measured. Microbial antibodies were analysed against enteroviruses (coxsackievirus B4), hepatitis A virus, Helicobacter pylori and Toxoplasma gondii. Although total IgE level was higher in Russian Karelian children compared to their Finnish peers, the prevalence of allergen-specific IgE was lower among Russian Karelian children. The prevalence of microbial antibodies was, in turn, significantly more frequent in the Karelian children, reflecting the conspicuous difference in socio-economic background factors. Microbial infections were associated with lower risk of allergic sensitization in Russian Karelian children, enterovirus showing the strongest protective effect in a multivariate model. The present findings support the idea that exposure to certain infections, particularly in childhood, may protect from the development of atopy. Enterovirus infections represent a new candidate to the list of markers of such a protective environment. However, possible causal relationship needs to be confirmed in further studies.
Notes
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PubMed ID
17302731 View in PubMed
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Analysis of Ag-presenting cells in the conjunctiva during the development of experimental immune-mediated blepharoconjunctivitis.

https://arctichealth.org/en/permalink/ahliterature50604
Source
Curr Eye Res. 2004 Oct-Nov;29(4-5):277-86
Publication Type
Article
Author
Akemi Ozaki
Atsuki Fukushima
Waka Ishida
Olga Zinchuk
Kazuyo Fukata
Yoshihiro Hayashi
Hideaki Enzan
Masaru Takata
Hideo Yagita
Hisayuki Ueno
Author Affiliation
Department of Ophthalmology, Kochi Medical School, Kohasu, Oko-cho, Nankoku City 783-8505, Japan.
Source
Curr Eye Res. 2004 Oct-Nov;29(4-5):277-86
Language
English
Publication Type
Article
Keywords
Animals
Antigen-Presenting Cells - immunology
Antigens, CD - metabolism
Antigens, CD86
Blepharitis - immunology
Blotting, Western
Cell Count
Conjunctiva - immunology
Conjunctivitis, Allergic - immunology
Extracellular Signal-Regulated MAP Kinases - metabolism
Flow Cytometry
Histocompatibility Antigens Class II - metabolism
Immunoenzyme Techniques
Immunophenotyping
Lymphocyte Activation
Macrophages - immunology
Male
Membrane Glycoproteins - metabolism
Microscopy, Confocal
Models, Theoretical
Ovalbumin - immunology
Phosphorylation
Rats
Rats, Inbred BN
T-Lymphocytes - immunology
Abstract
PURPOSE: The aim of this study was to investigate the phenotypes of antigen (Ag) presenting cells (APCs) in the conjunctiva during the development of experimental immune-mediated blepharoconjunctivitis (EC), which serves as a model for investigation of severe types of human allergic conjunctivitis. METHODS: Brown Norway rats treated by ovalbumin (OVA) were used in this study. To confirm the restriction of MHC class II by OVA-specific T cells, monoclonal Abs against MHC class II were added to the conventional proliferation assay. To evaluate the MHC class II expression in the conjunctiva during the development of EC, an immunohistochemical analysis, either as the single or double staining, was performed. Conjunctival fibroblast cell lines were established from naive rats and the MHC class II expression was evaluated by flow cytometric analysis. To examine the roles of costimulatory molecules, OVA-specific T cells were stimulated with anti-TcR Ab and anti-CD28 Ab and then subjected for Western blotting to evaluate the ERK phosphorylation. Finally, in vivo expression of B7 molecules was examined immunohistochemically. RESULTS: OVA-specific T cells recognized OVA in the context of MHC class II. MHC class II was expressed in conjunctival macrophages but not in fibroblasts. EC induction was accompanied by abundant infiltration of macrophages positive for MHC class II. MHC class II was also expressed in conjunctival epithelial cells by EC induction. Stimulation from CD28 was necessary for ERK phosphorylation. B7-2, but not B7-1, was expressed in the conjunctiva. CONCLUSION: Conjunctival macrophages may represent a major source of APCs for the induction of EC in the conjunctiva.
PubMed ID
15590473 View in PubMed
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91 records – page 1 of 10.