bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhaled cornstarch glove powder increases latex‐induced airway hyper‐sensitivity in guinea‐pigs
Authors: Barbara J. , Santais M.‐C. , Levy D. A. , Ruff F. , Leynadier F. 
Published: June 2004

SummaryBackground
Breathing is one of the most important modes of sensitization to natural rubber latex (NRL) for health‐care workers, a group most at risk. Cornstarch powder (CSp) from medical powdered NRL gloves is known to be an allergen carrier, and sensitization to NRL can occur by inhaling airborne particles from such gloves.Objective
The aim of this study was to demonstrate, using an experimental model, which CSp may act as an adjuvant in NRL‐induced airway hyper‐responsiveness.Methods
Guinea‐pigs were exposed to aerosolized NRL‐contaminated CSp or to NRL in saline solution for 1 h every day for 2 weeks. The control groups were exposed either to CSp or to saline alone. An additional group of guinea‐pigs was exposed to aerosolized ovalbumin (OVA) in saline. Three weeks after the last exposure, specific bronchial challenges were performed. In addition, Specific IgG and IgG1 in sera and thromboxane (Tx) B2 levels in bronchoalveolar lavage fluid (BALF) were measured.Results
The NRL challenge caused significant bronchospasm in the animals that had been exposed to NRL compared with those in the control groups (P<0.02). Guinea‐pigs exposed to OVA also demonstrated a significant bronchospasm after OVA challenge (P<0.001). The guinea‐pigs that had inhaled NRL‐contaminated CSp had a significantly higher bronchoconstriction level than those that had inhaled NRL alone (P<0.02). Specific IgG and IgG1 were undetectable in sera from all groups, whereas significant amounts of TxB2 (P<0.001) were found in the lungs of the guinea‐pigs exposed to NRL or OVA.Conclusion
Inhaling CSp increases the airway response to NRL. The fact that specific IgG and IgG1 were not detected might be the result of an immune response limited to the airways. This finding is supported by a significant increase of TxB2 level in the BALF of sensitized guinea‐pigs.
Effect of glucocorticosteroids on tumour necrosis factor‐α‐induced intercellular adhesion molecule‐1 expression in cultured primary human nasal epithelial cells
Authors: Shirasaki H. , Watanabe K. , Kanaizumi E. , Sato J. , Konno N. , Narita S. , Himi T. 
Published: June 2004

SummaryObjective
In order to confirm the direct effect of glucocorticosteroids on epithelial intercellular adhesion molecule‐1 (ICAM‐1) expression, we examined ICAM‐1 expression on primary cultured human nasal epithelial cells (HNECs) at both protein and mRNA levels.Material and methods
HNECs were stimulated with recombinant human TNF‐α (20 pg/mL–20 ng/mL) for specified time periods (0, 12, 24, and 48 h) and ICAM‐1 mRNA and the soluble ICAM‐1 (sICAM‐1) concentrations were measured by quantitative RT‐PCR and ELISA, respectively. We also evaluated surface expression of ICAM‐1 by flow cytometry 48 h after stimulation and determined the effect of dexamethasone (DEX) on TNF‐α‐induced ICAM‐1 expression.Results
Significant increases in ICAM‐1 gene expression in HNECs were initially detected at 24 h, peaking at 48 h after the stimulation. The TNF‐mediated‐ICAM‐1 mRNA and ICAM‐1 surface expression at 48 h was significantly inhibited by co‐incubation with human recombinant soluble TNF receptor I. Similarly, TNF‐α‐induced release sICAM‐1 occurred in a time‐ and concentration‐dependent manner. DEX 10−6 m attenuated the TNF‐α‐induced ICAM‐1 expression at mRNA and protein levels.Conclusions
Our finding suggests a potential role for topical steroids in allergic rhinitis in suppressing inflammatory reactions in the nasal mucosa by regulating ICAM‐1 expression on nasal epithelium.
Urinary 3‐bromotyrosine and 3‐chlorotyrosine concentrations in asthmatic patients: lack of increase in 3‐bromotyrosine concentration in urine and plasma proteins in aspirin‐induced asthma after intravenous aspirin challenge
Authors: Mita H. , Higashi N. , Taniguchi M. , Higashi A. , Kawagishi Y. , Akiyama K. 
Published: June 2004

SummaryBackground
Eosinophil peroxidase and myeloperoxidase halogenate tyrosine residues in plasma proteins and generate 3‐bromotyrosine (BY) and 3‐chlorotyrosine (CY), respectively.Objectives
(1) To estimate urinary concentrations of BY and CY in asthmatic patients. (2) To investigate BY concentration in relation to urinary leukotriene E4 (LTE4) concentration in order to evaluate the activation of eosinophils in patients with aspirin‐induced asthma (AIA).Methods
BY and CY were quantified with a gas chromatograph‐mass spectrometer using 13C‐labelled compounds as internal standards.Results
(1) Activation of eosinophils and neutrophils by immobilized IgG1 induced preferential formation of BY and CY, respectively. (2) A significantly higher concentration of BY was observed in the urine from asthmatic patients than in that from healthy control subjects (45±21.7 vs. 22.6±10.8 ng/mg‐creatinine, P<0.01). CY concentration was also elevated in the urine from asthmatic patients (4.4±3.2 vs. 1.5±1.0 ng/mg‐creatinine, P<0.01). (3) After intravenous aspirin challenge of aspirin‐induced asthmatic patients, the concentration of BY in urine did not significantly change. No significant change was also observed in the ratio of BY concentration to total tyrosine concentration in plasma proteins. In contrast, the concentration of urinary LTE4 significantly increased after the intravenous aspirin challenge.Conclusion
Determination of BY and CY concentrations may be useful for monitoring the activation of eosinophils and neutrophils in asthmatic patients, respectively. After aspirin challenge of AIA patients, the increased concentration of urinary LTE4 did not accompany changes in BY concentration in both urine and plasma proteins. These results may preclude the activation of eosinophils after aspirin challenge in patients with AIA.
Characteristics of patients with seasonal allergic rhinitis and concomitant asthma
Authors: Bousquet J. , Boushey H. A. , Busse W. W. , Canonica G. W. , Durham S. R. , Irvin C. G. , Karpel J. P. , Van Cauwenberge P. , Chen R. , Iezzoni D. G. , Harris A. G. 
Published: June 2004

SummaryBackground
Allergic rhinitis and asthma often co‐exist and appear to produce a continuum of airway disease, but whether the clinical characteristics of asthma in patients with seasonal rhinitis differ from those of persistent asthma has not been examined.Objective
The aim of this retrospective study was to characterize the clinical features of patients with seasonal allergic rhinitis with concomitant asthma and to compare them with those in patients with persistent asthma.Methods
The patient populations for this study were derived from nine prospective, placebo‐controlled planned clinical trials of similar design. Six studies (958 patients) enrolled patients with seasonal allergic rhinitis and concomitant asthma; three (607 patients) involved patients with persistent asthma. In all studies, patients were excluded from oral corticosteroid therapy in the preceding 3 months, and from inhaled corticosteroids in the preceding month.Results
Patients with seasonal rhinitis and asthma had a significantly (P<0.001) higher total asthma symptom score than those with persistent asthma. In particular, cough was three times more severe. The need for β2‐agonist as a rescue medication and the ratio of forced expiratory volume in 1 s/forced vital capacity (FVC) were similar in the two groups whereas forced expiratory fraction 25–75%/FVC was significantly (P<0.02) reduced in the persistent asthmatics. Asthma and nasal symptom severity scores were correlated in patients with seasonal rhinitis and asthma (P<0.0001).Conclusions
Patients with seasonal allergic rhinitis and concomitant asthma appear to differ from those with persistent asthma. A prospective study should be designed to discover whether patients with seasonal rhinitis and asthma may represent a distinct nosological entity, ‘allergic airway disease’.
Airway function and nasal inflammation in seasonal allergic rhinitis and asthma
Authors: Ciprandi G. , Cirillo I. , Vizzaccaro A. , Milanese M. , Tosca M. A. 
Published: June 2004

SummaryBackground
Allergic rhinitis (AR) and asthma are frequently associated and characterized by a Th2‐dependent inflammation. Nasal and bronchial obstruction may be objectively measured.Objective
The aim of this study was to evaluate the relationships among upper and lower airway function and nasal inflammation in subjects with seasonal allergic rhinitis (SAR) and asthma.Methods
Twenty out‐patients (12 males and eight females, mean age: 23.4+3.6 years) with SAR and asthma were evaluated during the pollen season. All of them showed a moderate–severe grade of nasal obstruction. Total symptom score, rhinomanometry, spirometry, nasal lavage, and nasal scraping were obtained in all subjects. Eosinophils were counted by conventional staining; IL‐4 and IFN‐γ were measured by immunoassay on fluids recovered from nasal lavage.Results
Functional parameters, i.e. nasal airflow and forced expiratory volume in 1 s (FEV1), were correlated with nasal eosinophils (R2>0.83, P<0.001). Inflammatory parameters, i.e. eosinophils were correlated with immunological parameters, i.e. IL‐4 and IFN‐γ levels (R2=0.93, P<0.001). Nasal symptoms were correlated with nasal airflow (ρ=−0.71, P0.01) and eosinophils (ρ=0.72, P<0.01). Nasal airflow was correlated with FEV1 (r=0.89, P<0.0001).Conclusions
This study demonstrates the close connection between Th2 cytokines and eosinophil infiltration in the nose. There is also clear evidence concerning the relationships between eosinophils infiltration and cytokines levels. Nasal eosinophils can be regarded as the most important predictors of upper and lower airway functions. These findings constitute first evidence of a relationship among nasal Th2‐related inflammation and nasal and bronchial airflow in patients with SAR and asthma.
Functional expression of high‐affinity receptor for immunoglobulin E on mast cells precedes that of tryptase during differentiation from human bone marrow‐derived CD34 progenitors cultured in the presence of stem cell factor and interleukin‐6
Authors: Shimizu Y. , Suga T. , Maeno T. , Aoki F. , Tsukagoshi H. , Kawata T. , Sakai K. , Narita T. , Takahashi T. , Ishikawa S. , Morishita Y. , Nakajima T. , Hara F. , Miura T. , Kurabayashi M. 
Published: June 2004

SummaryBackground
CD34+ progenitor cells develop into tryptase+, CD117+ mast cells when cultured in the presence of recombinant human stem cell factor (rhSCF). However, spontaneous IgE receptor (FcɛRI) expression during human mast cell development is not well examined.Objective
Here, the expression and function of FcɛRI in and on human bone marrow‐derived mast cells (HBMMCs) during development were investigated.Methods and Results
At 4 weeks of culture, predominant cells expressed high‐affinity IgE receptor α chain (FcɛRIα) on the cell surface determined by flow cytometry, but CD117 was less expressed. Immunocytochemistry with antitryptase mAb and anti‐FcɛRIα mAb revealed intracellular and surface expression of FcɛRIα at 2 weeks of culture, but tryptase was less expressed. FcɛRIα mRNA transcript preceded that of tryptase mRNA at 2 weeks of culture determined by real‐time RT‐PCR, and FcɛRIα, FcɛRIβ, FcɛRIγ, and tryptase mRNA increased along with differentiation. FcɛRIα cross‐link on HBMMC and 4‐week‐old mast cells/mast cell precursors induced the release of IL‐5 and granulocyte macrophage‐colony stimulating factor, which was enhanced by rhSCF.Conclusion
These data indicated that HBMMC constitutively and spontaneously expressed functional FcɛRI subunits at the early stage of differentiation, probably because of the differences in the ability and functional property of progenitors.
Permeability of synthetic and feather pillows to live house dust mites and house dust
Authors: Siebers R. , Nam H.‐S. , Crane J. 
Published: June 2004

SummaryBackground
Previous studies have demonstrated significantly higher house dust mite (HDM) allergen levels from synthetic pillows, compared to feather pillows. Reasons for these differences could be lower permeability of feather pillow coverings to allergen in dust, greater HDM penetration of synthetic pillow covering, or both.Objectives
To determine the permeability of synthetic and feather pillow coverings to live HDMs and house dust.Methods
Twenty live adult HDMs were seeded on top of two types of synthetic pillow covering (one standard polyester and one newer polyester/cotton type) and one type of feather pillow coverings with adequate food supply below in sealed culture dishes, kept at 23°C and 70% relative humidity. After 24 and 48 h live HDM numbers remaining on top of the coverings were enumerated microscopically. Three aliquots of fine house dust (each in triplicate) were placed on top of the synthetic and feather pillow coverings, shaken gently for 30 min and penetrated dust was collected and weighed.Results
After 24 h, all 20 HDMs had penetrated the standard synthetic pillow coverings, and no HDMs had penetrated either the feather pillow or the new synthetic pillow coverings after 24 or 48 h. Dust permeability (% of applied dust) for the standard synthetic, new type synthetic and feather pillow coverings were 0.88%, 0.07%, and 0.07%, respectively. This compared to 0.02% for a commercial occlusive pillow cover.Conclusions
These findings of total permeability of standard synthetic pillow coverings to live HDMs, and their greater permeability to house dust could explain their reported higher HDM allergen levels, compared to feather pillow coverings. Newer types of synthetic pillow coverings are similar to feather pillow coverings in their permeability to live HDMs and house dust.
Interleukin‐18 levels in induced sputum are reduced in asthmatic and normal smokers
Authors: McKay A. , Komai‐Koma M. , MacLeod K. J. , Campbell C. C. , Kitson S. M. , Chaudhuri R. , Thomson L. , McSharry C. , Liew F. Y. , Thomson N. C. 
Published: June 2004

SummaryBackground
IL‐18 is a cytokine which is known to have an important role in the development of a Th1 lymphocyte response. As such, it may have a regulatory role in asthma by modifying Th2 lymphocyte responses. Cigarette smoking may amplify the airway inflammation associated with asthma.Objective
This study investigated if IL‐18 could be detected in induced sputum from asthmatics and normal subjects and if smoking altered IL‐18 levels.Methods
Induced sputum was obtained from asthmatic (31 smokers, 35 non‐smokers) and normal (20 smokers, 20 non‐smokers) subjects. All smokers had a smoking history of 15 pack years. IL‐18 levels in sputum supernatant were measured by ELISA. IL‐18 mRNA expression and cellular localization were assessed by quantitative PCR and immunocytochemistry, respectively.Results
Smoking was associated with a significant reduction in IL‐18 levels (median (interquartile range) – smokers 20 (0–102) pg/mL vs. non‐smokers 358 (50–876) pg/mL, P<0.001). This was more pronounced in asthmatics (smokers, 47 (40–64) pg/mL vs. non‐smokers, 530 (30–1484) pg/mL; P<0.001) than in normal subjects (smokers, 25 (0–78) pg/mL vs. non‐smokers, 247 (50–656) pg/mL; P<0.01). Within each of the smoking and non‐smoking groups there was no significant difference in IL‐18 levels between asthmatic and normal subjects. There was no correlation between sputum IL‐18 levels and any specific cell type in the sputum samples nor serum IgE levels. IL‐18 mRNA expression was reduced in asthmatic smokers compared with non‐smokers. IL‐18 production was localized to sputum macrophages by immunocytochemistry.Conclusions
IL‐18 is detectable in induced sputum samples from both asthmatic and normal subjects. Cigarette smoking significantly reduces sputum IL‐18 levels. This effect is more pronounced in asthmatics than in normal subjects.
The expression of stem cell factor and c‐kit receptor in human asthmatic airways
Authors: Al‐Muhsen S. Z. , Shablovsky G. , Olivenstein R. , Mazer B. , Hamid Q. 
Published: June 2004

SummaryBackground
Asthmatic airways are characterized by infiltration with a variety of inflammatory cells such as mast cells and eosinophils. Stem cell factor (SCF) is an important activating and chemotactic factor for both mast cells and eosinophils. In addition, it is a critical growth and differentiation factor for mast cells.Objectives
To investigate the contribution of SCF to the pathogenesis of asthma, we examined the expression of SCF and its receptor c‐kit in bronchial biopsies and bronchoalveolar lavage (BAL) specimens obtained from asthmatic subjects (n=13) and non‐asthmatic control subjects (n=10).Methods
SCF and c‐kit were detected by in situ hybridization (ISH) and immunocytochemistry (ICC). In order to phenotype the cells expressing SCF and c‐kit in asthmatic tissue and BAL cells, combined ISH and ICC were also performed.Results
There was a significant difference (P<0.001) in the SCF mRNA expression in asthmatic airway epithelium (70.38±12.33% positive cells) compared with controls (12.7±17.21% positive cells). There was also a significant difference in subepithelial SCF‐mRNA expression, being higher in asthmatics (P<0.001). A significant difference was also found in c‐kit receptor mRNA expression in asthmatic biopsies both in epithelium (P<0.001) and subepithelium (P<0.05) compared with controls. ICC results were consistent with the ISH for both SCF and c‐kit receptor from asthmatics and controls. The SCF and c‐kit receptor mRNA and immunoreactivity in cells recovered from bronchial washing were also significantly higher in asthmatics compared with controls (P<0.05). While SCF expression was localized predominantly in the epithelial layer in bronchial biopsy tissues, alveolar macrophages were found to be the major source of SCF in bronchial washing from asthmatic subjects.Conclusion
The results of this study demonstrate the increased expression of SCF and its receptor, c‐kit within human asthmatic airways, which suggests an important role of this cytokine in the pathophysiology of asthma.
Cow's milk‐specific immunoglobulin E levels as predictors of clinical reactivity in the follow‐up of the cow's milk allergy infants
Authors: García‐Ara M. C. , Boyano‐Martínez M. T. , Díaz‐Pena J. M. , Martín‐Muñoz M. F. , Martín‐Esteban M. 
Published: June 2004

SummaryBackground
IgE‐mediated cow's milk proteins (CMPs) allergy shows a tendency to disappear with age. The sooner tolerance is detected, the earlier the substitute diets can be suspended and the quicker family emotional hardship is alleviated.Objective
To analyse the specific IgE levels to cow's milk and its proteins, which help to separate tolerant from no tolerant children in the follow‐up of infants with allergy to cow's milk.Patients and methods
Sixty‐six infants diagnosed with IgE‐mediated allergy to CMPs were included in this prospective follow‐up study. Periodic reassessments were carried out every 6 months until they were 2‐years old and then, annually, until tolerance arose or until the last reassessment in which tolerance had not been achieved. Non‐tolerant infants were followed, at least, for a period of 3 years. In each visit, the same skin tests and determination of specific IgE (CAP System FEIA) for milk and its proteins were carried out. The open challenge test was repeated unless a clear transgression to milk, which came to be positive, had taken place within the previous 3 months in each of the follow‐up visits. Specific IgE levels to milk and its proteins, in different moments of the follow‐up were analysed by means of the receiver‐operating characteristic curve to predict clinical reactivity.Results
Throughout the follow‐up 45 (68%) infants became tolerant. The follow‐up mean for tolerant infants was 21.2 months whereas for non‐tolerant infants it was 58 months. The specific IgE levels which were predictors of the clinical reactivity (positive predictive value (PPV)90%), grew as the age of the infants increased: 1.5, 6 and 14 kUA/L for milk in the age range 13–18 and 19–24 months and in the third year, respectively. Specific IgE levels to casein: 0.6, 3 and 5 kUA/L, respectively, predicted clinical reactivity (PPV90%) in the different analysed moments of the follow‐up. The cut‐off points: 2.7, 9 and 24 kUA/L for milk and 2, 4.2 and 9 kUA/L for casein, respectively, predicted clinical reactivity with an accuracy 95% corresponding to a specificity of 90%.Conclusions
Monitorization of specific IgE concentration for milk and casein by means of the CAP system in allergic children to CMPs allows us to predict, to a high degree of probability, clinical reactivity. Age factor must be taken into account to evaluate the specific IgE levels which are predictors of tolerance or clinical reactivity.
ADAM33 polymorphism: association with bronchial hyper‐responsiveness in Korean asthmatics
Authors: Lee J. H. , Park H.‐S. , Park S. W. , Jang A. S. , Uh S. T. , Rhim T. , Park C.‐S. , Hong S.‐J. , Holgate S. T. , Holloway J. W. , Shin H. D. 
Published: June 2004

SummaryBackground
A disintegrin and metalloprotease 33 (ADAM33) is expressed in the lung by fibroblasts and bronchial smooth muscle cells. Given its structure and cellular provenance, ADAM33 may be associated with airway remodelling and bronchial hyper‐responsiveness. Single nucleotide polymorphisms (SNPs) and haplotypes of the ADAM33 gene have previously been associated with asthma susceptibility in the Caucasian population.Objective and Methods
To assess whether genetic variants of ADAM33 are related to asthma in a Korean population, we conducted an association study of the ADAM33 gene with asthma susceptibility, bronchial hyper‐reactivity and serum IgE in Korean asthmatics (n=326) and normal controls (n=151). Five of the 14 polymorphisms originally reported to be associated with asthma development (S1 G>A, T1 T>C, V‐1 C>A, V1 T>A, V4 C>G) were genotyped using single base extension and electrophoresis. Haplotypes and their frequencies were inferred using the algorithm implemented by the software Arlequin. Allele frequencies of each SNP and haplotypes were compared between the patients and the normal controls using logistic regression analysis.Results
There was no significant difference in the distribution of SNPs and the six haplotypes between asthmatics and normal controls. All single SNPs and six haplotypes in ADAM33 were also analysed for the association with level of PC20 using general linear models. The distribution of the T1 T>C SNP and one haplotype (ht4: GCGG) showed significant association with log‐transformed PC20 methacholine level in the asthma patients (P=0.03 and 0.0007, respectively, using a co‐dominant model).Conclusion
Polymorphism of ADAM33 may contribute to development of BHR in asthma.