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Activation of the immune system and systemic immune-complex deposits in Brown Norway rats with dental amalgam restorations.

https://arctichealth.org/en/permalink/ahliterature72544
Source
J Dent Res. 1998 Jun;77(6):1415-25
Publication Type
Article
Date
Jun-1998
Author
P. Hultman
U. Lindh
P. Hörsted-Bindslev
Author Affiliation
Department of Health and Environment, Linköping University, Sweden.
Source
J Dent Res. 1998 Jun;77(6):1415-25
Date
Jun-1998
Language
English
Publication Type
Article
Keywords
Analysis of Variance
Animals
Antibody Formation - drug effects
Antigen-Antibody Complex - analysis - blood
Autoimmune Diseases - chemically induced
Autoimmunity
Body Burden
Comparative Study
Copper - analysis
Dental Amalgam - toxicity
Dinitrobenzenes
Female
Immune Complex Diseases - chemically induced
Immunoglobulin E - blood
Laminin
Lymphocyte Activation - drug effects
Mercury - analysis - blood - pharmacokinetics
Rats
Rats, Inbred BN
Rats, Inbred Lew
Research Support, Non-U.S. Gov't
Silver - analysis
Spectrum Analysis, Mass
Statistics, nonparametric
Tissue Distribution
Abstract
Dental amalgam restorations are a significant source of mercury exposure in the human population, but their potential to cause systemic health effects is highly disputed. We examined effects on the immune system by giving genetically mercury-susceptible Brown Norway (BN) rats and mercury-resistant Lewis (LE) rats silver amalgam restorations in 4 molars of the upper jaw, causing a body burden similar to that described in human amalgam-bearers (from 250 to 375 mg amalgam/kg body weight). BN rats with amalgam restorations, compared with control rats given composite resinous restorations, developed a rapid activation of the immune system, with a maximum 12-fold increase of the plasma IgE concentration after 3 wks (p 0.05). After 12 wks, BN rats with amalgam restorations showed significantly increased (p spleen > cerebrum occipital lobe > cerebellum > liver > thymus, and the tissue silver concentration was significantly (p
PubMed ID
9649170 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 responses in Brown Norway rats following inhalation sensitization and challenge with trimellitic anhydride.

https://arctichealth.org/en/permalink/ahliterature80614
Source
Toxicol Sci. 2006 Dec;94(2):322-9
Publication Type
Article
Date
Dec-2006
Author
Zhang Xing-Dong
Andrew Michael E
Hubbs Ann F
Siegel Paul D
Author Affiliation
Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505, USA.
Source
Toxicol Sci. 2006 Dec;94(2):322-9
Date
Dec-2006
Language
English
Publication Type
Article
Keywords
Administration, Inhalation
Airway Resistance - drug effects - physiology
Allergens - immunology - toxicity
Animals
Antibodies, Anti-Idiotypic - blood
Bronchi - drug effects - pathology
Bronchial Hyperreactivity - chemically induced - immunology - pathology
Bronchial Provocation Tests
Female
Immunoglobulin E - blood - immunology
Inhalation Exposure
Phthalic Anhydrides - immunology - toxicity
Plethysmography, Whole Body
Rats
Rats, Inbred BN
Respiratory Hypersensitivity - chemically induced - immunology - pathology
Specific Pathogen-Free Organisms
Abstract
Trimellitic anhydride (TMA) is a cause of asthma in man. Dose-dependent TMA-specific IgE, histopathology, and airway responses after sensitization by inhalation were examined in the Brown Norway rat. Rats were exposed to 0.04, 0.4, 4, or 40 mg/m3 TMA aerosol for 10 min, once a week, over 10 weeks. All lower exposures were, subsequently, rechallenged to 40 mg/m3 TMA aerosol. All rats received a sham exposure 1 week prior to the first TMA exposure. Following the sham exposure and weekly after each TMA exposure, TMA-specific IgE and both early-phase airway response (EAR) and late-phase airway response (LAR) were measured using enhanced pause (Penh). All rats sensitized by 40 mg/m3 TMA developed specific IgE, EAR, and LAR to one or more of the challenges to 40 mg/m3 TMA. TMA of 4 mg/m3 induced a much lower, but stable, specific IgE response. EAR and LAR were observed only after a 40 mg/m3 TMA rechallenge in this group, but it was much larger than that observed in the 40 mg/m3 TMA-sensitized and challenged group. Exposure-dependent histopathological changes noted included eosinophilic granulomatous interstitial pneumonia, perivascular eosinophil infiltrates, bronchial-associated lymphoid tissue hyperplasia, and peribronchiolar plasma cell infiltrates.
PubMed ID
16982671 View in PubMed
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Alveolar macrophages have a dual role in a rat model for trimellitic anhydride-induced occupational asthma.

https://arctichealth.org/en/permalink/ahliterature15039
Source
Toxicol Appl Pharmacol. 2006 Feb 15;211(1):20-9
Publication Type
Article
Date
Feb-15-2006
Author
Dingena L Valstar
Marcel A Schijf
Frans P Nijkamp
Gert Storm
Josje H E Arts
C Frieke Kuper
Nanne Bloksma
Paul A J Henricks
Author Affiliation
Department of Pharmacology and Pathophysiology, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Sorbonnelaan 16, 3584 CA, Utrecht, The Netherlands.
Source
Toxicol Appl Pharmacol. 2006 Feb 15;211(1):20-9
Date
Feb-15-2006
Language
English
Publication Type
Article
Keywords
Allergens
Analysis of Variance
Animals
Asthma - blood - chemically induced - immunology
Comparative Study
Cytokines - analysis
Disease Models, Animal
Female
Immunoglobulin E - blood
Lung - immunology
Macrophages, Alveolar - immunology
Occupational Diseases - blood - chemically induced - immunology
Phthalic Anhydrides
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Respiratory Function Tests
Statistics, nonparametric
Abstract
Occupational exposure to low molecular weight chemicals, like trimellitic anhydride (TMA), can result in occupational asthma. Alveolar macrophages (AMs) are among the first cells to encounter inhaled compounds. These cells can produce many different mediators that have a putative role in asthma. In this study, we examined the role of AMs in lung function and airway inflammation of rats exposed to TMA. Female Brown Norway rats were sensitized by dermal application of TMA or received vehicle alone on days 0 and 7. One day before challenge, rats received intratracheally either empty or clodronate-containing liposomes to deplete the lungs of AMs. On day 21, all rats were challenged by inhalation of TMA in air. Lung function parameters were measured before, during, within 1 h after, and 24 h after challenge. IgE levels and parameters of inflammation and tissue damage were assessed 24 h after challenge. Sensitization with TMA led to decreased lung function parameters during and within 1 h after challenge as compared to non-sensitized rats. AM depletion alleviated the TMA-induced drop in lung function parameters and induced a faster recovery compared to sham-depleted TMA-sensitized rats. It also decreased the levels of serum IgE 24 h after challenge, but did not affect the sensitization-dependent increase in lung lavage fluid IL-6 and tissue TNF-alpha levels. In contrast, AM depletion augmented the TMA-induced tissue damage and inflammation 24 h after challenge. AMs seem to have a dual role in this model for TMA-induced occupational asthma since they potentiate the immediate TMA-induced decrease in lung function but tended to dampen the TMA-induced inflammatory reaction 24 h later.
PubMed ID
15992840 View in PubMed
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CD8+ T cells modulate late allergic airway responses in Brown Norway rats.

https://arctichealth.org/en/permalink/ahliterature57532
Source
J Immunol. 1999 Nov 15;163(10):5574-81
Publication Type
Article
Date
Nov-15-1999
Author
M. Suzuki
R. Taha
D. Ihaku
Q. Hamid
J G Martin
Author Affiliation
Meakins-Christie Laboratories, Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada.
Source
J Immunol. 1999 Nov 15;163(10):5574-81
Date
Nov-15-1999
Language
English
Publication Type
Article
Keywords
Adoptive Transfer
Animals
Bronchial Provocation Tests
Bronchoalveolar Lavage Fluid - cytology - immunology
CD8-Positive T-Lymphocytes - immunology - metabolism - transplantation
Cytokines - biosynthesis
Flow Cytometry
Hypersensitivity, Delayed - immunology
Immunoglobulin E - blood
Leukocytes, Mononuclear - cytology - immunology
Lymph Nodes - cytology - immunology - metabolism
Lymphocyte Count
Lymphocyte Subsets - cytology - immunology
Male
Ovalbumin - blood - immunology
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Spleen - cytology - immunology - metabolism
Abstract
To test the hypothesis that CD8+ T cells may suppress the allergen-induced late airway response (LAR) and airway eosinophilia, we examined the effect of administration of Ag-primed CD8+ T cells on allergic airway responses, bronchoalveolar lavage (BAL) leukocytes, and mRNA expression for cytokines (IL-4, IL-5, and IFN-gamma) in OVA-sensitized Brown Norway rats. On day 12 postsensitization to OVA, test rats were administered 2 million CD8+ T cells i.p. isolated from either the cervical lymph nodes (LN group; n = 8) or the spleen (Spl group; n = 6) of sensitized donors. On day 14, test rats were challenged with aerosolized OVA. Control rats were administered PBS i.p. on day 12, and challenged with OVA (n = 10) or BSA (n = 6) on day 14. The lung resistance was measured for 8 h after challenge. BAL was performed at 8 h. Cytospin slides of BAL were analyzed for major basic protein by immunostaining and for cytokine mRNA by in situ hybridization. The LAR was significantly less in the LN group (1.8 +/- 0.5 U; p
PubMed ID
10553086 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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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 CD8+gammadelta T cells on late allergic airway responses and airway inflammation in rats.

https://arctichealth.org/en/permalink/ahliterature57418
Source
J Allergy Clin Immunol. 2003 Sep;112(3):547-55
Publication Type
Article
Date
Sep-2003
Author
Susumu Isogai
Alexandra Rubin
Karim Maghni
David Ramos-Barbon
Rame Taha
Yasuyuki Yoshizawa
Qutayba Hamid
James G Martin
Author Affiliation
Meakins Christie Laboratories, Department of Medicine, McGill University, 3623 St Urbain, Montreal, Quebec, Canada H2X 2P2.
Source
J Allergy Clin Immunol. 2003 Sep;112(3):547-55
Date
Sep-2003
Language
English
Publication Type
Article
Keywords
Adoptive Transfer
Allergens - administration & dosage
Animals
CD8-Positive T-Lymphocytes - immunology
Cytokines - biosynthesis - genetics
Eosinophilia - immunology
Immunoglobulin E - blood
Interferon Type II - biosynthesis - genetics
Interleukin-4 - biosynthesis - genetics
Male
Models, Immunological
Ovalbumin - administration & dosage - immunology
RNA, Messenger - genetics - metabolism
Rats
Rats, Inbred BN
Receptors, Antigen, T-Cell, gamma-delta - metabolism
Research Support, Non-U.S. Gov't
Respiratory Hypersensitivity - etiology - immunology
T-Lymphocyte Subsets - immunology
Abstract
BACKGROUND: Gamma-delta (gammadelta) T cells regulate immune responses to foreign protein at mucosal surfaces. Whether they can modify allergen-induced early (EAR) and late airway responses (LAR) is unknown. OBJECTIVE: We have tested the hypothesis that the CD8+ subtype of gammadelta T cells decreases allergen-induced LAR and airway eosinophilia in the rat. METHODS: Brown Norway rats were administered, intraperitoneally, 3.5 x 10(4) lymph node CD8+gammadelta T cells from naive or sensitized rats. The recipients were sensitized to ovalbumin (OVA) in Al(OH)(3) 3 days after cell transfer and challenged with aerosolized OVA 14 days later. Serum IgE was measured before allergen challenge. After challenge, lung resistance was monitored for 8 hours and then bronchoalveolar lavage (BAL) was analyzed for eosinophil major basic protein (MBP), IL-4, IL-5, IL-13, and IFN-gamma messenger RNA-expressing cells. RESULTS: gammadelta T cells from naive donors significantly decreased LAR in OVA-challenged sensitized rats, whereas MBP(+) eosinophils were decreased by both gammadelta T cells from naive and sensitized donors. EAR and serum IgE levels were unchanged. The expression of IL-4, IL-5, and IL-13 by BAL cells of gammadelta T cell recipients was attenuated compared with OVA-challenged controls. This was accompanied by an increase in the expression of IFN-gamma. CONCLUSIONS: Our results are consistent with a suppressive role of CD8+gammadelta T cells on allergic airway responses. However, only gammadelta T cells from naive donors inhibit LAR.
PubMed ID
13679814 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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Effects of transforming growth factor-beta and formula feeding on systemic immune responses to dietary beta-lactoglobulin in allergy-prone rats.

https://arctichealth.org/en/permalink/ahliterature82418
Source
Pediatr Res. 2006 May;59(5):650-5
Publication Type
Article
Date
May-2006
Author
Penttila Irmeli
Author Affiliation
Child Health Research Institute, North Adelaide, South Australia, Australia 5006. irmeli.penttila@adelaide.edu.au
Source
Pediatr Res. 2006 May;59(5):650-5
Date
May-2006
Language
English
Publication Type
Article
Keywords
Animals
Animals, Newborn
Antibody Specificity
Chymases
Cytokines - genetics - metabolism
Eosinophils - drug effects - immunology - pathology
Female
Ileum - drug effects - immunology - pathology
Immune Tolerance
Immunoglobulin E - blood
Immunoglobulin G - blood
Infant Formula - administration & dosage
Lactoglobulins - immunology
Mast Cells - drug effects - enzymology - immunology - pathology
Milk - immunology
Milk Hypersensitivity - drug therapy - immunology - pathology
Pregnancy
RNA, Messenger - genetics - metabolism
Rats
Rats, Inbred BN
Recombinant Proteins - administration & dosage
Serine Endopeptidases - metabolism
Spleen - immunology
Th1 Cells - drug effects - immunology
Transforming Growth Factor beta - administration & dosage
Abstract
Early nutritional events have the potential to affect health outcomes in later life including the development of allergy. Food allergy is usually the first manifestation of allergy. Breast-feeding has been associated with a protective effect against the development of allergy, but the evidence is contradictory and the mechanisms involved are not clear. We hypothesize that milk cytokines, such as transforming growth factor beta (TGF-beta), play a role in regulating immune responses to dietary antigens. Using a rat pup model of gastrostomy feeding, the immune response profile, at weaning and post-weaning, of allergy-prone Brown Norway rats fed formula supplementation with TGF-beta was assessed. We show that feeding formula to allergy-prone rat pups results in increased total IgE immunoglobulin, beta-lactoglobulin (BLG) IgG1 antibody, and mucosal mast cell activation, as measured by serum rat mast cell protease II (RMCPII) levels in the gut. Supplementation of formula with physiological levels of TGF-beta down-regulated the BLG IgG1 response as well as total IgE and mucosal mast cell activation. Supplementation of formula also resulted in an increase in Th1 cytokines, interleukin (IL)-18, IL-12p40, IL-12p35, and interferon gamma (IFN-gamma) and an increase in IL-10. In conclusion, TGF-beta supplementation of formula moved the immune response profile of allergy prone (Th2 type) rat pups toward a Th1 profile in the suckling period. Importantly, this immune profile persisted after weaning when TGF-beta was no longer present in the diet.
PubMed ID
16627876 View in PubMed
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24 records – page 1 of 3.