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14 records – page 1 of 2.

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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Atopy patch test with different vehicles and allergen concentrations: an approach to standardization.

https://arctichealth.org/en/permalink/ahliterature35371
Source
J Allergy Clin Immunol. 1995 Mar;95(3):677-84
Publication Type
Article
Date
Mar-1995
Author
U. Darsow
D. Vieluf
J. Ring
Author Affiliation
Department of Dermatology and Allergology, University Hospital Eppendorf, University of Hamburg, Germany.
Source
J Allergy Clin Immunol. 1995 Mar;95(3):677-84
Date
Mar-1995
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Allergens - administration & dosage - immunology
Child
Child, Preschool
Comparative Study
Dermatitis, Atopic - diagnosis - immunology
Dose-Response Relationship, Drug
Female
Humans
Male
Middle Aged
Patch Tests - standards
Pollen - immunology
Radioallergosorbent Test
Sensitivity and specificity
Vehicles - administration & dosage
Abstract
BACKGROUND: In some patients with atopic eczema, eczematous skin lesions can be induced by patch testing with aeroallergens. METHODS: To establish a standardized system for the atopy patch test (APT), 36 patients with atopic eczema, four patients with rhinoconjunctivitis and 10 healthy control subjects were epicutaneously tested with allergen extracts from house dust mite, cat dander, and grass pollen. APTs were performed on nonabraded, uninvolved skin with 1000 and 10,000 protein nitrogen units (PNU)/gm allergen in petrolatum or hydrogel. Reactions were evaluated after 48 and 72 hours and compared with skin prick and specific serum IgE (CAP-RAST; Pharmacia, Uppsala, Sweden). RESULTS: After 48 hours, 57 clear-cut positive reactions with eczematous, often follicle-bound, appearance were diagnosed from a total of 432 test sites. Seventy-two percent of these positive reactions in patients with atopic eczema developed with 10,000 PNU/gm and 28% with 1000 PNU/gm. Sixty-seven percent of reactions were elicited with allergens in petrolatum versus 33% when hydrogel was used as vehicle. Allergen-specific concordances of APT (10,000 PNU/gm, petrolatum) ranged from 0.39 to 0.53 (prick test) and 0.42 to 0.69 (CAP-RAST). In healthy control subjects and patients with rhinoconjunctivitis without atopic eczema, no clear-cut positive APT reaction was seen. CONCLUSIONS: Petrolatum as vehicle and an allergen concentration higher than 1000 PNU/gm may lead to improved APT results on unchanged skin. In the future, the clinical relevance of an IgE-mediated sensitization for eczematous skin lesions may be evaluated by the APT.
PubMed ID
7897150 View in PubMed
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Characterization of allergen-induced bronchial hyperresponsiveness and airway inflammation in actively sensitized brown-Norway rats.

https://arctichealth.org/en/permalink/ahliterature57758
Source
J Allergy Clin Immunol. 1991 Dec;88(6):951-60
Publication Type
Article
Date
Dec-1991
Author
W. Elwood
J O Lötvall
P J Barnes
K F Chung
Author Affiliation
Department of Thoracic Medicine, National Heart and Lung Institute, London, England.
Source
J Allergy Clin Immunol. 1991 Dec;88(6):951-60
Date
Dec-1991
Language
English
Publication Type
Article
Keywords
Acetylcholine - administration & dosage
Aerosols
Airway Resistance - drug effects
Allergens - administration & dosage - immunology
Animals
Bronchial Hyperreactivity - etiology - immunology
Bronchial Provocation Tests - methods
Bronchitis - etiology - immunology
Bronchoalveolar Lavage Fluid - cytology
Comparative Study
Dose-Response Relationship, Immunologic
Immunization - methods
Male
Rats - immunology
Research Support, Non-U.S. Gov't
Time Factors
Abstract
Bronchial responsiveness to inhaled acetylcholine (ACh) and inflammatory cell recruitment in bronchoalveolar lavage fluid (BALF) were studied in inbred Brown-Norway rats actively sensitized to, and later exposed to, ovalbumin (OA). We examined animals 21 days after initial sensitization at 18 to 24 hours, or 5 days after a single challenge, or after the last of seven repeated exposures administered every 3 days. BALF was examined as an index of inflammatory changes within the lung. Animals repeatedly exposed to OA aerosols had an increased baseline lung resistance and a significant increase in bronchial responsiveness to inhaled ACh compared to control animals at both 18 to 24 hours and 5 days after the last OA exposure. Sensitized animals receiving a single OA aerosol also demonstrated bronchial hyperresponsiveness (BHR) to inhaled ACh (p less than 0.01) at 18 to 24 hours of a similar order as the multiple-exposed group. There was a significant increase in eosinophils, lymphocytes, and neutrophils in BALF at 18 to 24 hours but not at 5 days after single or multiple exposure to OA aerosol in the sensitized groups. Control animals demonstrated no changes in bronchial responsiveness, although a small but significant increase in inflammatory cells was observed compared to saline-only treated animals. There was a significant correlation between bronchial responsiveness and eosinophil counts in the BALF in the single allergen-exposed group (Rs = 0.68; p less than 0.05). We conclude that (1) BHR after allergen exposure in sensitized rats is associated with the presence of pulmonary inflammation but persists despite the regression of inflammatory cells in BALF after multiple OA exposures, and (2) this rat model has many characteristics of human allergen-induced BHR.
PubMed ID
1744366 View in PubMed
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Comparative microarray analysis and pulmonary changes in Brown Norway rats exposed to ovalbumin and concentrated air particulates.

https://arctichealth.org/en/permalink/ahliterature90256
Source
Toxicol Sci. 2009 Mar;108(1):207-21
Publication Type
Article
Date
Mar-2009
Author
Heidenfelder Brooke L
Reif David M
Harkema Jack R
Cohen Hubal Elaine A
Hudgens Edward E
Bramble Lori A
Wagner James G
Morishita Masako
Keeler Gerald J
Edwards Stephen W
Gallagher Jane E
Author Affiliation
Human Studies Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA.
Source
Toxicol Sci. 2009 Mar;108(1):207-21
Date
Mar-2009
Language
English
Publication Type
Article
Keywords
Air Pollutants - toxicity
Allergens - administration & dosage - immunology
Analysis of Variance
Animals
Bronchoalveolar Lavage Fluid - chemistry - immunology
Bronchopneumonia - metabolism - pathology
Gene Expression - drug effects
Inflammation - immunology
Lung - drug effects - immunology - metabolism - pathology
Male
Oligonucleotide Array Sequence Analysis
Ovalbumin - administration & dosage - immunology
Particulate Matter - administration & dosage - toxicity
Principal Component Analysis
Rats
Respiratory Hypersensitivity - metabolism - pathology
Respiratory Mucosa - drug effects - immunology - metabolism - pathology
Abstract
The interaction between air particulates and genetic susceptibility has been implicated in the pathogenesis of asthma. The overall objective of this study was to determine the effects of inhalation exposure to environmentally relevant concentrated air particulates (CAPs) on the lungs of ovalbumin (ova) sensitized and challenged Brown Norway rats. Changes in gene expression were compared with lung tissue histopathology, morphometry, and biochemical and cellular parameters in bronchoalveolar lavage fluid (BALF). Ova challenge was responsible for the preponderance of gene expression changes, related largely to inflammation. CAPs exposure alone resulted in no significant gene expression changes, but CAPs and ova-exposed rodents exhibited an enhanced effect relative to ova alone with differentially expressed genes primarily related to inflammation and airway remodeling. Gene expression data was consistent with the biochemical and cellular analyses of the BALF, the pulmonary pathology, and morphometric changes when comparing the CAPs-ova group to the air-saline or CAPs-saline group. However, the gene expression data were more sensitive than the BALF cell type and number for assessing the effects of CAPs and ova versus the ova challenge alone. In addition, the gene expression results provided some additional insight into the TGF-beta-mediated molecular processes underlying these changes. The broad-based histopathology and functional genomic analyses demonstrate that exposure to CAPs exacerbates rodents with allergic inflammation induced by an allergen and suggests that asthmatics may be at increased risk for air pollution effects.
PubMed ID
19176365 View in PubMed
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Dose-response and time course of specific IgE and IgG after single and repeated topical skin exposure to dry trimellitic anhydride powder in a Brown Norway rat model.

https://arctichealth.org/en/permalink/ahliterature15360
Source
Allergy. 2002 Jul;57(7):620-6
Publication Type
Article
Date
Jul-2002
Author
X D Zhang
D K Murray
D M Lewis
P D Siegel
Author Affiliation
Natioanl Institute for Occupational Safety and Health, Morgantown, WV 26505, USA.
Source
Allergy. 2002 Jul;57(7):620-6
Date
Jul-2002
Language
English
Publication Type
Article
Keywords
Administration, Topical
Allergens - administration & dosage - immunology
Animals
Antibody Specificity
Disease Models, Animal
Dose-Response Relationship, Immunologic
Humans
Hypersensitivity - immunology
Immunoglobulin E - blood
Immunoglobulin G - blood
Phthalic Anhydrides - administration & dosage - immunology
Rats
Rats, Sprague-Dawley
Abstract
BACKGROUND: Trimellitic anhydride (TMA)-induced occupational asthma is thought to be associated with its ability to acylate proteins and to induce production of TMA-specific immunoglobulin (Ig)E. Though the respiratory tract is considered to be a major exposure route leading to airway sensitization, the potential role of dermal exposure producing asthmatic sensitization is not known. The present study examines the ability of dry TMA powder to sensitize Brown Norway rats when applied, topically, to the skin. METHODS: A patch of hair was carefully clipped with scissors on the rat's back. Dry TMA powder (0.3, 1.25, 5 and 20 mg) was administered on days 0, 7, 14 and 21, and the area occluded with surgical tape overnight after each application. Residual powder recovered from the occluded skin was analyzed by proton nuclear magnetic resonance and was still predominantly TMA. Circulating anti-TMA IgE and IgG were measured by ELISA. RESULTS: TMA elicited dose-dependent production of specific IgE and IgG. Specific antibodies were detectable 2 weeks after the first TMA exposure and peaked between 3 and 4 weeks. CONCLUSION: The data suggest that topical skin exposure to dry TMA powder can induce allergic/immunological sensitization as demonstrated by the production of specific antibodies.
PubMed ID
12100303 View in PubMed
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Evidence for an atypical receptor mediating the augmented bronchoconstrictor response to adenosine induced by allergen challenge in actively sensitized Brown Norway rats.

https://arctichealth.org/en/permalink/ahliterature57463
Source
Br J Pharmacol. 2002 Feb;135(3):685-96
Publication Type
Article
Date
Feb-2002
Author
J P Hannon
B. Tigani
C. Wolber
I. Williams
L. Mazzoni
C. Howes
J R Fozard
Author Affiliation
Research Department, Novartis Pharma AG, CH-4002 Basel, Switzerland.
Source
Br J Pharmacol. 2002 Feb;135(3):685-96
Date
Feb-2002
Language
English
Publication Type
Article
Keywords
Adenosine - pharmacology - physiology
Adenosine-5'-(N-ethylcarboxamide) - pharmacology
Adjuvants, Immunologic - administration & dosage
Airway Resistance - drug effects - physiology
Allergens - administration & dosage - immunology
Animals
Bronchial Provocation Tests - methods
Bronchoconstriction - drug effects - physiology
Dose-Response Relationship, Drug
Immunization
Injections, Subcutaneous
Intubation, Intratracheal
Lung - drug effects - physiology
Male
Ovalbumin - administration & dosage - immunology
Rats
Rats, Inbred BN
Receptors, Purinergic P1 - agonists - antagonists & inhibitors - physiology
Vasodilator Agents - pharmacology
Abstract
The bronchoconstrictor response to adenosine is markedly and selectively increased following ovalbumin (OA) challenge in actively sensitized, Brown Norway rats. We present a pharmacological analysis of the receptor mediating this response. Like adenosine, the broad-spectrum adenosine receptor agonist, NECA, induced dose-related bronchoconstriction in actively sensitized, OA-challenged animals. In contrast, CPA, CGS 21680 and 2-Cl-IB-MECA, agonists selective for A(1) A(2A) and A(3) receptors, respectively, induced no, or minimal, bronchoconstriction. Neither the selective A(1) receptor antagonist, DPCPX, nor the selective A(2A) receptor antagonist, ZM 241385, blocked the bronchoconstrictor response to adenosine. MRS 1754, which has similar affinity for rat A(2B) and A(1) receptors, failed to block the bronchoconstrictor response to adenosine despite blockade of the A(1) receptor-mediated bradycardia induced by NECA. 8-SPT and CGS 15943, antagonists at A(1), A(2A), and A(2B) but not A(3) receptors, inhibited the bronchoconstrictor response to adenosine. However, the degree of blockade (approximately 3 fold) did not reflect the plasma concentrations, which were 139 and 21 times greater than the K(B) value at the rat A(2B) receptor, respectively. Adenosine and NECA, but not CPA, CGS 21680 or 2-Cl-IB-MECA, induced contraction of parenchymal strip preparations from actively sensitized OA-challenged animals. Responses to adenosine could not be antagonized by 8-SPT or MRS 1754 at concentrations >50 times their affinities at the rat A(2B) receptor. The receptor mediating the bronchoconstrictor response to adenosine augmented following allergen challenge in actively sensitized BN rats cannot be categorized as one of the four recognized adenosine receptor subtypes.
PubMed ID
11834616 View in PubMed
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Identification of contact sensitizers by animal assay.

https://arctichealth.org/en/permalink/ahliterature57916
Source
Contact Dermatitis. 1980 Jan;6(1):46-50
Publication Type
Article
Date
Jan-1980
Author
B. Magnusson
Source
Contact Dermatitis. 1980 Jan;6(1):46-50
Date
Jan-1980
Language
English
Publication Type
Article
Keywords
Administration, Topical
Allergens - administration & dosage - immunology
Animals
Biological Assay
Dermatitis, Atopic - chemically induced - immunology
Dermatitis, Contact - etiology - immunology
Guinea Pigs
Immunization
Injections, Intradermal
Patch Tests
Abstract
Guinea pig testing constitutes the first step in evaluating the allergenicity of new chemicals and products. Some of the most commonly used animal predictive tests are reviewed. The guinea pig maximization test, which is the recommended test method in Sweden, is described in detail and the interpretation of results obtained with this test is discussed. In the guinea pig maximization test the sensitization capacity of a substance is examined by the use of maximized conditions for the exposure, i.e. the potential ability of the material to induce a contact allergy is determined. The extent to which an allergen causes contact dermatitis in exposed persons depends on the mode of use and various environmental factors.
PubMed ID
7398258 View in PubMed
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Induced changes in total serum IgE concentration in the Brown Norway rat: potential for identification of chemical respiratory allergens.

https://arctichealth.org/en/permalink/ahliterature15416
Source
J Appl Toxicol. 2002 Jan-Feb;22(1):1-11
Publication Type
Article
Author
E V Warbrick
R J Dearman
I. Kimber
Author Affiliation
Syngenta Central Toxicology Laboratory, Alderley Park, Macclesfield, Cheshire SK10 4TJ, UK.
Source
J Appl Toxicol. 2002 Jan-Feb;22(1):1-11
Language
English
Publication Type
Article
Keywords
Administration, Topical
Air Pollutants, Environmental - immunology
Air Pollutants, Occupational - immunology
Allergens - administration & dosage - immunology
Animals
Dinitrochlorobenzene - administration & dosage - immunology
Female
Immunoglobulin E - blood - drug effects
Immunoglobulin G - blood - drug effects
In Vitro
Kinetics
Lymph Nodes - cytology - immunology
Mice
Mice, Inbred BALB C
Phthalic Anhydrides - administration & dosage - immunology
Rats
Research Support, Non-U.S. Gov't
Respiratory Hypersensitivity - immunology
Abstract
A variety of chemicals can cause sensitization of the respiratory tract and occupational asthma that may be associated with IgE antibody production. Topical exposure to chemical respiratory allergens such as trimellitic anhydride (TMA) has been shown previously to induce increases in the total serum concentration of IgE in BALB/c strain mice. Contact allergens such as 2,4-dinitrochlorobenzene (DNCB), which apparently lack respiratory sensitizing potential, fail to provoke similar changes. However, it became apparent with time that there was some inter-animal variation in constitutive and inducible IgE levels. We have now examined the influence of topical exposure to TMA and DNCB on serum IgE levels in the Brown Norway (BN) rat. Such animals can be bled serially and thus it is possible to perform longitudinal analyses of changes in serum IgE concentration. The kinetics of IgE responses therefore can be followed on an individual animal basis, allowing discrimination between transient and sustained increases in serum IgE concentration. Rats (n = 5) were exposed on shaved flanks to 50% TMA, to 1% DNCB (concentrations that elicit comparable immune activation with respect to draining lymph node cellularity and proliferation) or to vehicle alone. Total IgE was measured by enzyme-linked immunosorbent assay in serum samples taken prior to and 14-42 days following initial exposure. Those animals having high pre-existing IgE levels (>1.0 microg ml(-1)) were excluded from subsequent analyses. The levels of serum IgE in the majority of rats exposed to DNCB or vehicle alone remained relatively stable throughout the duration of all the experiments conducted, although some animals displayed transient increases in serum IgE. Only TMA treatment was associated with a significant and sustained increase in the level of serum IgE in the majority of experiments. The elevated concentrations of IgE induced by topical exposure to TMA are persistent, the results reported here demonstrating that induced changes in IgE are maximal or near maximal at approximately 35 days, with a significant increase in IgE demonstrable for at least 42 days following the initiation of exposure. Interestingly, although TMA and DNCB at the test concentrations used were found to be of comparable overall immunogenicity with regard to lymph node activation and the induction of lymph node cell proliferation, there were apparent differences in humoral immune responses. Thus, not only did exposure to TMA stimulate increases in total serum IgE concentration and the production of specific IgE antibody, but also a more vigorous IgG antibody response was provoked by TMA compared with DNCB. These data suggest that the measurement of induced changes in serum IgE concentration in the BN strain of rat is able to differentiate between different classes of chemical allergen. Given the inter-animal variation in IgE production, it would be prudent to incorporate a concurrent assessment of responses induced by treatment with TMA as a positive control against which to assess the activity of other test materials.
PubMed ID
11807923 View in PubMed
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Involvement of alpha-4 integrins in allergic airway responses and mast cell degranulation in vivo.

https://arctichealth.org/en/permalink/ahliterature57560
Source
Am J Respir Crit Care Med. 1998 Oct;158(4):1127-33
Publication Type
Article
Date
Oct-1998
Author
M. Hojo
K. Maghni
T B Issekutz
J G Martin
Author Affiliation
Meakins-Christie Laboratories, McGill University, Montreal, Quebec; and the Izaak Walton Killam Children's Hospital, Grace Centre, Dalhousie University, Halifax, Nova Scotia, Canada.
Source
Am J Respir Crit Care Med. 1998 Oct;158(4):1127-33
Date
Oct-1998
Language
English
Publication Type
Article
Keywords
Adjuvants, Immunologic - administration & dosage
Airway Resistance - immunology
Allergens - administration & dosage - immunology
Animals
Anti-Allergic Agents - immunology
Antibodies, Monoclonal - therapeutic use
Antigens, CD - immunology
Antigens, CD29 - immunology
Bile - chemistry
Bronchoalveolar Lavage Fluid - chemistry
Cell Adhesion Molecules - immunology
Cell Degranulation - immunology
Histamine - analysis
Immunization
Integrin alpha4
Integrin alpha4beta1
Integrins - immunology
Leukotriene E4 - analogs & derivatives - analysis
Male
Mast Cells - immunology
Ovalbumin - administration & dosage - immunology
Rats
Rats, Inbred BN
Receptors, Lymphocyte Homing - immunology
Receptors, Very Late Antigen - immunology
Research Support, Non-U.S. Gov't
Respiratory Hypersensitivity - immunology
Serine Endopeptidases - analysis
Virulence Factors, Bordetella - administration & dosage
Abstract
Antibodies against integrins have been shown to inhibit allergic airway responses. The purpose of this study was to test the hypothesis that the beta1 integrin, very late antigen-4 (VLA-4), is involved in mast cell activation triggered by allergen exposure in sensitized animals. To do this we studied Brown Norway rats that were sensitized to ovalbumin (OA; 1 mg subcutaneously) using Bordetella pertussis as an adjuvant. Two weeks later rats were challenged with OA, pulmonary resistance (RL) was determined, and the concentrations of histamine and tryptase in bronchoalveolar lavage fluid and N-acetyl-leukotriene (LT)E4 in bile were measured. Pretreatment with a monoclonal antibody against VLA-4 (TA-2) attenuated the early response after OA challenge (342.9 +/- 24.4% baseline RL versus 153.3 +/- 19.4%; p
PubMed ID
9769271 View in PubMed
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Pholcodine stimulates a dramatic increase of IgE in IgE-sensitized individuals. A pilot study.

https://arctichealth.org/en/permalink/ahliterature82996
Source
Allergy. 2006 Jan;61(1):49-55
Publication Type
Article
Date
Jan-2006
Author
Florvaag E.
Johansson S G O
Oman H.
Harboe T.
Nopp A.
Author Affiliation
Laboratory of Clinical Biochemistry, Haukeland University Hospital, Bergen, Norway.
Source
Allergy. 2006 Jan;61(1):49-55
Date
Jan-2006
Language
English
Publication Type
Article
Keywords
Adult
Allergens - administration & dosage - immunology
Antitussive Agents - administration & dosage - immunology
Codeine - administration & dosage - analogs & derivatives
Enzyme-Linked Immunosorbent Assay
Female
Galectin 3 - immunology
Humans
Hypersensitivity - immunology - physiopathology
Immunization
Immunoglobulin E - biosynthesis - immunology
Leukocytes, Mononuclear - drug effects - immunology
Male
Morphine - administration & dosage
Morpholines - administration & dosage
Neuromuscular Blocking Agents - administration & dosage - immunology
Pilot Projects
Sensitivity and specificity
Succinylcholine - administration & dosage
Abstract
BACKGROUND: A previous study showed a relation between pholcodine (PHO) consumption, prevalence of IgE-sensitization to PHO, morphine (MOR) and suxamethonium (SUX) and anaphylaxis to neuromuscular blocking agents (NMBA). The purpose of this pilot study was to explore the effect on IgE production, in IgE-sensitized and nonsensitized individuals, of exposure to cough syrup and environmental chemicals containing PHO, MOR and SUX related allergenic structures. METHODS: Serum concentrations of IgE and IgE antibodies to PHO, MOR and SUX allergens measured by ImmunoCAP (Pharmacia Diagnostics, Uppsala, Sweden) were followed after intake of cough syrup, or exposure to confectionary and other household chemicals containing various amounts of substances cross-reacting with PHO, MOR and SUX. RESULTS: Cough syrup containing PHO gave, in sensitized individuals, within 1-2 weeks, an increase of IgE of 60-105 times and of IgE antibodies to PHO, MOR and SUX in the order of 30-80 times. The tested confectionary did not have any similar stimulating effect but seemed to counteract the expected decrease of IgE. No effect was seen in nonsensitized individuals. The PHO stimulated IgE showed a nonspecific binding to ImmunoCAP with common allergens and glycine background ImmunoCAP that was up to 10-fold higher than that of monomeric myeloma-IgE at twice the concentration. CONCLUSIONS: It seems as cough syrups containing PHO have a most remarkable IgE boostering effect in persons IgE-sensitized to PHO, MOR and SUX related allergens. Household chemicals containing such allergenic epitopes seem capable of some, minor, stimulation.
PubMed ID
16364156 View in PubMed
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14 records – page 1 of 2.