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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

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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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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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
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Correlation of ovalbumin of egg white components with allergic diseases in children.

https://arctichealth.org/en/permalink/ahliterature277582
Source
J Microbiol Immunol Infect. 2016 Feb;49(1):112-8
Publication Type
Article
Date
Feb-2016
Author
Yang-Te Lin
Chih-Te Wu
Jing-Long Huang
Ju-Hui Cheng
Kuo-Wei Yeh
Source
J Microbiol Immunol Infect. 2016 Feb;49(1):112-8
Date
Feb-2016
Language
English
Publication Type
Article
Keywords
Adolescent
Age Factors
Allergens - immunology
Child
Child, Preschool
Egg White
Female
Food Hypersensitivity - epidemiology
Humans
Immunoassay
Immunoglobulin E - blood
Infant
Male
Ovalbumin - immunology
Sweden
Abstract
Immunoglobulin E (IgE)-mediated food allergy, such as egg white allergy, is common in young children (
PubMed ID
24662019 View in PubMed
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Dose-dependent recruitment of CD25+ and CD26+ T cells in a novel F344 rat model of asthma.

https://arctichealth.org/en/permalink/ahliterature77142
Source
Am J Physiol Lung Cell Mol Physiol. 2007 Jun;292(6):L1564-71
Publication Type
Article
Date
Jun-2007
Author
Skripuletz Thomas
Schmiedl Andreas
Schade Jutta
Bedoui Sammy
Glaab Thomas
Pabst Reinhard
von Hörsten Stephan
Stephan Michael
Author Affiliation
Department of Functional and Applied Anatomy, Medical School of Hannover, Germany.
Source
Am J Physiol Lung Cell Mol Physiol. 2007 Jun;292(6):L1564-71
Date
Jun-2007
Language
English
Publication Type
Article
Keywords
Animals
Antigens, CD26 - metabolism
Asthma - immunology - pathology
Bronchoalveolar Lavage Fluid - cytology - immunology
Bronchoconstriction - immunology
CD4-Positive T-Lymphocytes - immunology - metabolism
CD8-Positive T-Lymphocytes - immunology - metabolism
Disease Models, Animal
Dose-Response Relationship, Immunologic
Eosinophils - immunology
Immunoglobulin E - blood
Immunophenotyping
Interleukin-2 Receptor alpha Subunit - metabolism
Lung - cytology - immunology
Ovalbumin - immunology - pharmacology
Rats
Rats, Inbred F344
T-Lymphocytes, Regulatory - immunology - metabolism
Abstract
The ovalbumin (OVA)-induced airway inflammation in rats is a commonly used model to explore the pathobiology of asthma. However, its susceptibility varies greatly between rat strains, and presently Brown Norway (BN) rats are preferentially used. Since recruitment of T cells to the lungs depends on the CD26 (dipeptidyl peptidase IV, DPPIV) expression, Fischer 344 strain (F344) rats are a highly relevant rat strain, in particular because CD26-deficient substrains are available. To establish a F344 rat model of asthma, we challenged F344 rats using different doses of aerosolized antigen (0%, 1%, 2.5%, 5%, and 7.5% OVA) and compared these effects with intratracheal instillation of OVA (1.5 mg/0.3 ml). Asthmoid responsiveness was determined by analysis of early airway responsiveness (EAR), antigen-specific IgE levels, as well as airway inflammation including the composition of T cell subpopulations in the bronchoalveolar lavage (BAL) and lung tissue with special respect to the T cell activation markers CD25 and CD26. Even low allergen doses caused allergen-specific EAR and increases of antigen-specific IgE levels. However, EAR and IgE levels did not increase dose dependently. Higher concentrations of OVA led to a dose-dependent increase of several immunological markers of allergic asthma including an influx of eosinophils, T cells, and dendritic cells. Interestingly, a dose-dependent increase of CD4(+)/CD25(+)/CD26(+) T cells was found in the lungs. Summarizing, we established a novel F344 rat model of aerosolized OVA-induced asthma. Thereby, we found a dose-dependent recruitment of cellular markers of allergic asthma including the activated CD4(+)/CD25(+)/CD26(+) T cell subpopulation, which has not been described in asthma yet.
PubMed ID
17351063 View in PubMed
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Effect of transforming growth factor-beta receptor I kinase inhibitor 2,4-disubstituted pteridine (SD-208) in chronic allergic airway inflammation and remodeling.

https://arctichealth.org/en/permalink/ahliterature81212
Source
J Pharmacol Exp Ther. 2006 Nov;319(2):586-94
Publication Type
Article
Date
Nov-2006
Author
Leung Sum Yee
Niimi Akio
Noble Alistair
Oates Timothy
Williams Alison S
Medicherla Satyanarayana
Protter Andrew A
Chung Kian Fan
Author Affiliation
National Heart and Lung Institute, Dovehouse St., London SW3 6LY, UK.
Source
J Pharmacol Exp Ther. 2006 Nov;319(2):586-94
Date
Nov-2006
Language
English
Publication Type
Article
Keywords
Acetylcholine - pharmacology
Activin Receptors, Type I - metabolism
Animals
Asthma - drug therapy
Bromodeoxyuridine - metabolism
Bronchi - drug effects
Chronic Disease
Dose-Response Relationship, Drug
Female
Immunoglobulin E - blood
Muscle, Smooth - drug effects
Ovalbumin - immunology
Protein-Serine-Threonine Kinases - antagonists & inhibitors
Pteridines - pharmacology
Rats
Rats, Inbred BN
Receptors, Transforming Growth Factor beta - metabolism
Smad2 Protein - analysis
Smad3 Protein - analysis
Transforming Growth Factor beta - physiology
Abstract
Transforming growth factor (TGF)-beta is a multifunctional regulator of cell growth and differentiation with both pro- and anti-inflammatory properties. We used an inhibitor of TGF-beta receptor I (TGF-betaRI) kinase, SD-208 (2,4-disubstituted pteridine, a ATP-competitive inhibitor of TGF-betaRI kinase), to determine the role of TGF-beta in airway allergic inflammation and remodeling. Brown-Norway rats sensitized and repeatedly exposed to ovalbumin (OVA) aerosol challenge were orally administered SD-208 twice daily, before each of six OVA exposures to determine the preventive effects, or only before each of the last three of six OVA exposures to investigate its reversal effects. SD-208 (60 mg/kg) reversed bronchial hyperresponsiveness (BHR) induced by repeated allergen exposure, but it did not prevent it. SD-208 prevented changes in serum total and OVA-specific IgE, but it did not reverse them. SD-208 had both a preventive and reversal effect on airway inflammation as measured by major basic protein-positive eosinophils and CD2(+) T-cell counts in mucosal airways, cell proliferation measured by 5-bromo-2'-deoxyuridine expression in airway smooth muscle (ASM) cells and epithelial cells, and goblet cell hyperplasia induced by repeated allergen challenges. There was a significant decrease in intracellular Smad2/3 expression. SD-208 did not significantly decrease the increased ASM thickness induced by allergen exposure. These findings support a proinflammatory and proremodeling role for TGF-beta in allergic airway inflammation. Inhibition of TGF-betaRI kinase activities by SD-208 may be a useful approach to the reversal of BHR and to the prevention and reversal of inflammatory and remodeling features of chronic asthma.
PubMed ID
16888081 View in PubMed
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The effects of IL-5 on airway physiology and inflammation in rats.

https://arctichealth.org/en/permalink/ahliterature15276
Source
J Allergy Clin Immunol. 2003 Mar;111(3):558-66
Publication Type
Article
Date
Mar-2003
Author
Sammy S Nag
Li Jing Xu
Qutayba Hamid
Paolo M Renzi
Author Affiliation
CHUM Research Center, Notre Dame Pavillion, University of Montreal, and the Meakins-Christie Laboratories, McGill University, Quebec, Canada.
Source
J Allergy Clin Immunol. 2003 Mar;111(3):558-66
Date
Mar-2003
Language
English
Publication Type
Article
Keywords
Animals
Blood Cells - pathology
Bronchoalveolar Lavage Fluid - cytology
Cell Differentiation - drug effects
Cytokines - genetics
Dose-Response Relationship, Drug
Eosinophils - pathology
Humans
Immunization
Immunoglobulin E - blood
Inflammation - physiopathology
Interleukin-5 - administration & dosage - pharmacology
Intubation, Intratracheal
Lung - metabolism
Lymphocyte Subsets - pathology
Male
Methacholine Chloride - pharmacology
Ovalbumin - immunology
RNA, Messenger - metabolism
Rats
Rats, Inbred BN
Recombinant Proteins - administration & dosage - pharmacology
Research Support, Non-U.S. Gov't
Respiratory System - drug effects - physiopathology
Respiratory Tract Diseases - physiopathology
Stem Cells - pathology
Abstract
BACKGROUND: There is evidence that the cytokine IL-5 is a prominent feature of airway inflammation in asthma. OBJECTIVE: The aim of this study was to determine whether exogenous IL-5 could cause changes in lung physiology, the early and late airway response after antigen challenge, and airway inflammation in rats that do not have a propensity to develop these changes after sensitization and challenge. METHOD AND RESULTS: Intratracheal administration of IL-5 to ovalbumin sensitized Brown Norway SSN rats increased the airway responsiveness to methacholine (AHR) 20 hours after administration of IL-5 at the same time as an increase in neutrophils occurred in the lung lavage. This effect was dose dependent and was not caused by endotoxin. Concurrent intratracheal administration of 50 ng of anti-IL-5 monoclonal antibody with 10 microg of recombinant human IL-5 decreased the AHR and neutrophil influx. Pretreatment with 3 microg of IL-5 had no effect on the early and late airway response or on AHR after ovalbumin challenge. However, IL-5 increased lung re-sistance 20 hours after antigen challenge. Although total lung cells and differential counts did not differ significantly 8 hours after antigen challenge, the blood lymphocyte CD4/CD8 ratio decreased in IL-5 pretreated rats (P
PubMed ID
12642837 View in PubMed
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No priming of the immune response in newborn brown norway rats dosed with ovalbumin in the mouth.

https://arctichealth.org/en/permalink/ahliterature51652
Source
Int Arch Allergy Immunol. 2003 Jan;130(1):66-72
Publication Type
Article
Date
Jan-2003
Author
C. Madsen
K. Pilegaard
Author Affiliation
Institute of Food Safety and Nutrition, Danish Veterinary and Food Administration, Søborg, Denmark. cm@fdir.dk
Source
Int Arch Allergy Immunol. 2003 Jan;130(1):66-72
Date
Jan-2003
Language
English
Publication Type
Article
Keywords
Animals
Animals, Newborn - immunology
Disease Models, Animal
Food Hypersensitivity - etiology
Immunoglobulin E - blood
Immunoglobulin G - blood
Ovalbumin - immunology
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Abstract
BACKGROUND: Other researchers have reported that the specific immune response to subsequent antigen challenge is primed in newborn mice or rats dosed orally by gavage. We wanted to investigate if priming of a subsequent specific IgE response could be achieved by dosing newborn rats orally with ovalbumin and if this method could be used in an animal model for food allergy. METHODS: Newborn Brown Norway rats were dosed with ovalbumin in the mouth (100 microg or 6 mg). As young adults, the animals were dosed by gavage for 35 days with 1 mg ovalbumin/day or once intraperitoneally with 100 microg. Control groups were dosed by gavage or intraperitoneally but not as neonates. Additionally, young adult rats were dosed with 1 mg ovalbumin/day in the mouth for 35 days. Sera from individual animals were analysed for specific IgE and specific IgG. RESULTS: In all experiments with neonatal rats the specific IgE and IgG responses were decreased compared to the control groups, however, not always reaching statistical significance. A statistical significant decrease in the specific immune response was found in young adult rats dosed in the mouth as compared to by gavage. CONCLUSIONS: Dosing Brown Norway rats with ovalbumin in the mouth as neonates do not prime the specific immune response. The decrease in immune response found in our experiments when dosing newborn animals in the mouth in opposition to the priming seen by others when dosing by intragastric intubation may be explained by a dissimilar antigen presentation when dosing includes both oral mucosa and gut.
PubMed ID
12576737 View in PubMed
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The strength of the OVA-induced airway inflammation in rats is strain dependent.

https://arctichealth.org/en/permalink/ahliterature15340
Source
Clin Exp Immunol. 2002 Sep;129(3):390-6
Publication Type
Article
Date
Sep-2002
Author
M N Hylkema
M O Hoekstra
M. Luinge
W. Timens
Author Affiliation
Department of Pathology and Laboratory Medicine, University Hospital Groningen, The Netherlands.
Source
Clin Exp Immunol. 2002 Sep;129(3):390-6
Date
Sep-2002
Language
English
Publication Type
Article
Keywords
Animals
Asthma - genetics - immunology
Cell Adhesion Molecules - metabolism
Cells, Cultured
Comparative Study
Cytokines - biosynthesis
Genetic Predisposition to Disease
Immunoglobulin E - blood
Inflammation - genetics - immunology
Kinetics
Leukocytes - immunology
Lung - cytology - immunology
Lymphocyte Subsets - classification - immunology
Male
Ovalbumin - immunology
Pulmonary Eosinophilia - immunology
Rats
Rats, Inbred BN
Rats, Sprague-Dawley
Research Support, Non-U.S. Gov't
Species Specificity
Abstract
To examine the influence of genetics on the OVA-induced allergic inflammatory response in lungs we compared rats that are genetically Th2-predisposed (Brown Norway, inbred) or not genetically predisposed (Sprague Dawley, outbred). Rats were sensitized with ovalbumin (OVA) and challenged four weeks later with OVA aerosol. Eighteen hours after challenge, lung tissue was studied for evaluation of numbers of eosinophils, neutrophils, macrophages and mast cells, as well as for expression of P-selectin, E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) on endothelial cells. From a separate portion of the pulmonary tissue, leucocytes were isolated to analyse numbers of IFNgamma and IL-4 producing cells (ELISPOT assay) and frequencies of T-cell subsets and B cells. We found increased numbers of eosinophils and neutrophils in the lung, an increased number of IL-4 producing cells in lung cell isolates and increased levels of serum (OVA- specific)-IgE in both rat strains. In addition, expression of E-selectin and ICAM-1 was up regulated in both rat strains whereas expression of VCAM-1 was only up regulated in the BN rat. Although the 'allergic' Th2 response to OVA was detectable in both rat strains, it was more pronounced in the BN rat than in the SD rat. However, the SD rat, which is not predisposed to respond in either a Th2 or Th1-like way, appeared capable of mounting an allergic response to OVA. This suggests that other factors than genetic contribute to allergic disease.
PubMed ID
12197878 View in PubMed
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10 records – page 1 of 1.