bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effects of carpet fresheners and other additives on the behaviour of indoor allergen assays
Authors: CHEW  , HIGGINS  , MILTON  , BURGE  
Published: March 2003

BackgroundChemical agents such as tannic acid and detergents have been shown to introduce non‐random bias in allergen measurement.ObjectiveWe investigated how several substances that are commonly found in floor dust (carpet fresheners, powdered pesticides, and table salt) affected immunoassays of purified standard allergens.MethodsThree sets of experiments were conducted to: (1) screen for interference with allergen enzyme‐linked immunosorbent assay (ELISA); (2) test for concentration‐response; and (3) assess the site‐of‐action of a given dust additive (i.e. the effect on allergen binding to primary or secondary antibody). The ELISAs are commercially available two‐site monoclonal antibody assays for Der p 1, Der f 1, and Fel d 1, and a monoclonal/polyclonal assay for Bla g 1. Outcomes are reported in terms of reaction rate (colour change per unit time), which is directly proportional to the amount of bound allergen.ResultsIn the initial screening experiments, carpet fresheners tended to decrease Der p 1 assay reaction rates, increase Der f 1 assay rates, and produce little change in Fel d 1 assay rates. Three carpet fresheners decreased Der p 1 assay rate responses in a concentration‐dependent manner. Two carpet fresheners noticeably increased Der f 1 assay reaction rates in both the screening and the concentration‐response tests. Powdered pesticides increased reaction rates in the Bla g 1 assays and increased the slope of the dilution curve compared with that of the purified allergen. Salt decreased the reaction rates of Bla g 1 assays at allergen concentrations greater than 0.01 U/mL. For each of the four allergens, the largest effects of dust additives occurred when secondary antibody binding was altered.ConclusionsSome common household dust components can introduce systematic error into immunoassays for arthropod allergens.
Enhanced basophil histamine release and neutrophil chemotactic activity predispose grain dust‐induced airway obstruction
Authors: PARK  , JUNG  , KANG  , NAHM  , CHO  , KIM  
Published: March 2003

BackgroundThe pathogenic mechanism of grain dust (GD)‐induced occupational asthma (OA) remains unclear.ObjectiveTo understand further the mechanism of GD‐induced OA.MethodsFifteen employees working in a same GD industry, complaining of work‐related respiratory symptoms, were enrolled and were divided into two groups according to the GD‐bronchoprovocation test (BPT) result: six positive responders were grouped as group III, nine negative responders as group II and five healthy controls as group I. Serum GD‐specific immunoglobulin (Ig)E (sIgE), specific IgG (sIgG) and specific IgG4 (sIgG4) antibodies were detected by enzyme‐linked immunosorbent assay. Basophil histamine release was measured by the autofluorometric method, and changes of serum neutrophil chemotactic activity were observed by the Boyden chamber method.ResultsFor clinical parameters such as degree of airway hyperresponsiveness to methacholine, duration of respiratory symptoms, exposure duration, and prevalences of serum sIgE, sIgG and sIgG4 antibodies, there were no significant differences between group II and III (P > 0.05, respectively). Serum neutrophil chemotactic activity increased significantly at 30 min and decreased at 240 min after the GD‐BPT in group III subjects (P < 0.05, respectively), while no significant changes were noted in group II subjects (P > 0.05). Basophil histamine release induced by GD was significantly higher in group III than those of group I or group II (P < 0.05, respectively), while minimal release of anti‐IgG4 antibodies was noted in all three groups.ConclusionsThese results suggest that enhanced basophil histamine release and serum neutrophil chemotactic activity might contribute to the development of GD‐induced occupational asthma.
Asthma, atopy and Chlamydia pneumoniae antibodies in adults
Authors: VON HERTZEN  , TÖYRYLÄ  , GIMISHANOV  , BLOIGU  , LEINONEN  , SAIKKU  , HAAHTELA  
Published: March 2003

BackgroundFactors involved in the development of inflammation and asthma in nonatopic subjects have remained largely obscure, although there is some evidence to suggest that certain infections may play a role.ObjectiveWe investigated the association between serological evidence of Chlamydia pneumoniae infection and asthma in adults, and the possible modifying effect of the patients' atopic status on this association.MethodsFour hundred and thirty consecutive patients who attended the hospital between 1992 and 1993 with symptoms suggestive of asthma, rhinitis or allergy were enrolled. Diagnostic procedures including lung function measurements and skin‐prick tests were performed in all patients. The patients with established asthma (n = 332) were divided into those with recent asthma (n = 224, onset 1985 onward) and longstanding asthma (n = 108, onset before 1985). The controls (n = 98) comprised all subjects who did not meet the criteria of asthma. Serum immunoglobulin (Ig)G, IgA and IgM antibodies to C. pneumoniae were measured by the microimmunofluorescence test.ResultsIn women, the prevalences of elevated IgG (a titre of ≥ 128) and IgA (≥ 32) antibody levels and the age‐adjusted geometric mean titres (GMT) of IgG and IgA antibodies were invariably highest among subjects with nonatopic longstanding asthma. Elevated IgG titres in women occurred in 11% of controls, in 28% of nonatopic recent onset asthmatics, and in 43% of asthmatics with nonatopic longstanding disease; for men the respective figures were 33, 50 and 64%. Logistic regression analysis controlling for age, sex and smoking showed that asthma was significantly associated with elevated IgG antibody levels to C. pneumoniae (odds ratio 3.3, 1.6–6.8 for longstanding asthma, 2.3, 1.2–4.4 for recent asthma, and among women only 4.2, 1.6–10.9 for longstanding asthma, and 3.0, 1.3–7.2 for recent asthma). When the atopics and nonatopics were analysed separately, an even stronger relationship in the nonatopics was obtained for longstanding asthma (6.0,2.1–17.1). In contrast, the relationship between atopic asthma, either recent or longstanding, and elevated IgG titres was not significant, indicating that asthma per se does not predispose to C. pneumoniae infection.ConclusionsAsthma was significantly associated with elevated IgG antibody levels to C. pneumoniae, and this association was strongest for nonatopic longstanding asthma.
Characterization of allergens from Penicillium oxalicum and P. notatum by immunoblotting and N‐terminal amino acid sequence analysis
Authors: SHEN  , LIN  , TAM  , WANG  , TZEAN  , HUANG  , HAN  
Published: March 2003

BackgroundPenicillium species are important causative agents of extrinsic bronchial asthma. However, little is known about the allergens of these ubiquitous fungal species. Objective    The object was to analyse the composition, the allergenic cross‐reactivity and the N‐terminal sequences of allergens from two prevalent airborne Penicillium species, P. oxalicum and P. notatum.MethodsThe allergenic composition and the immunoglobulin (Ig)E cross‐reactivity were analysed by immunoblot and immunoblot inhibition, respectively, using sera from asthmatic patients. The N‐terminal amino acid sequences of major allergens were determined by Edman degradation. Allergens identified were also characterized by immunoblotting using monoclonal antibody (MoAb) PCM39 against the alkaline serine proteinase major allergen of P. citrinum.ResultsAmong the 70 asthmatic sera tested, 18 (26%) and 17 (24%) had IgE immunoblot reactivity towards components of P. oxalicum and P. notatum, respectively. Major allergens (> 80% frequency of IgE‐binding) from both species are the 34 and 30 kDa proteins of P. oxalicum and the 34 and 32 kDa proteins of P. notatum. IgE cross‐reactivity among these major allergens and the 33 kDa major allergen of P. citrinum can be detected by immunoblot inhibition studies. The N‐terminal amino acid sequences of the 34 kDa allergen of P. oxalicum and of the 32 and the 28 kDa allergens of P. notatum share homology with sequences of the vacuolar serine proteinase from Aspergillus fumigatus. The N‐terminal amino acid sequence of the 34 kDa allergen of P. notatum shows sequence homology with that of alkaline serine proteinase from P. citrinum. Results obtained from immunoblotting showed that MoAb PCM39 reacted with the 34, 30 and 16 kDa IgE‐binding components of P. oxalicum, and with the 34, 32 and 28 kDa IgE‐binding components of P. notatum.ConclusionsResults obtained suggest that the 34 kDa major allergen of P. oxalicum may be a vacuolar serine proteinase. The 34 and the 32 kDa major allergens of P. notatum may be the alkaline and the vacuolar serine proteinases of P. notatum, respectively. The 30 and 16 kDa IgE‐binding components of P. oxalicum and the 28 kDa IgE‐binding component of P. notatum may be breakdown products of the 34 and the 32 kDa major vacuolar serine proteinase allergens of P. oxalicum and P. notatum, respectively.
Interleukin‐5 immunoreactivity and mRNA expression in gut mucosa from patients with food allergy
Authors: VANDEZANDE L. M. , WALLAERT B. , DESREUMAUX P. , TSICOPOULOS A. , LAMBLIN C. , TONNEL A. B. , JANIN A. 
Published: March 2003

Background and aimsEosinophils, mast cells and T lymphocytes are important cells in the allergic inflammatory process. These cells produce and are regulated by cytokines such as interleukin‐3 (IL‐3), interleukin‐5 (IL‐5) and granulocyte macrophage‐colony stimulating factor (GM‐CSF). We initiated this study to evaluate pathological abnormalities and to detect IL‐5 in the duodenal mucosa from patients with food allergy.MethodsEndoscopy duodenal biopsy specimens were obtained from seven food‐allergic patients, six atopic healthy controls and six nonatopic healthy controls. IL‐5 protein was evaluated by immunohistochemistry. Electron microscopy as well as double immunofluorescent staining were used to identify the labelled cells and to localize IL‐5. IL‐5 mRNA expression was evaluated by qualitative polymerase chain reaction.ResultsA significantly increased number of lymphocytes, mast cells and eosinophils was detected in the lamina propria in food‐allergic patients and, in lower number, in atopic controls. Immunostaining for IL‐5 was markedly positive in food‐allergic patients, slightly increased in atopic controls and negative in nonatopic controls. Ultrastructurally, in food‐allergic patients and in atopic controls, IL‐5 was localized in eosinophil granules, in the matrix of intact granules and at the periphery of altered granules. Double immunofluorescent staining was performed in food‐allergic patients and showed that 86.7% of IL‐5+ cells were eosinophils, and that IL‐5 was expressed by 24% of eosinophils. IL‐5 mRNA was expressed in food‐allergic patients but was not detected in atopic and nonatopic controls.ConclusionActivated eosinophils are involved in gut atopic reactions occurring in food allergy and are probably in part upregulated by their own local production of IL‐5.
Polymorphisms in the β2‐adrenoreceptor gene are associated with decreased airway responsiveness
Authors: Ramsay  , Hayden  , Tiller  , Burton  , Goldblatt  , Lesouef  
Published: March 2003

BackgroundThere are a number of candidate genes thought to play a role in the development of asthma. Polymorphisms at amino acid positions 16 (arginine to glycine) and 27 (glutamine to glutamic acid) of the β2‐adrenoreceptor (B2AR) gene are known to be functionally relevant and have been associated with more severe forms of asthma, nocturnal asthma and decreased airway responsiveness in asthmatic subjects.ObjectiveTo determine if these polymorphisms contribute to the development of asthma by investigating the associations between the polymorphisms at amino acid positions 16 and 27 of the B2AR gene and asthma‐related parameters in a large, phenotypically well‐characterized population which was unselected for asthma.MethodsSubjects (n = 332) were characterized using physiological assessments, immuno‐logical data and information obtained from questionnaire. PCR was used to generate a 229 base pair fragment spanning the mutations of interest. Genotype was determined using allele‐specific oligonucleotide hybridization and confirmed in 10% of the samples by direct sequencing. Multivariate analysis of the association between genotype and phenotype was then undertaken.ResultsHomozygotes for Glu27 were significantly less responsive to histamine than Gln27 homozygotes. In addition, Arg16 homozygotes were more likely to ‘wheeze during a cold’, in comparison with Gly16 homozygotes. However, there was no association between either polymorphism and physician‐diagnosed asthma, eczema, skin reactivity to common allergens or total and specific serum IgE levels. The two polymorphisms were found to be in significant linkage disequilibrium.ConclusionThe polymorphism at position 27 was associated with decreased airway responsiveness in the study population and the polymorphism at position 16 was associated with increased wheeze during respiratory infection, but neither was associated with physician‐diagnosed asthma or any of the other variables considered.
Cetirizine counter‐regulates interleukin‐8 release from human epithelial cells (A549)
Authors: Arnold R. , Rihoux J.‐P. , König W. 
Published: March 2003

BackgroundCetirizine, a H1‐receptor antagonist, exerts besides its well‐known anti‐allergic potential an array of anti‐inflammatory activities. In particular epithelial cells activated in the presence of cetirizine showed a reduced ICAM‐1 cell surface expression and a diminished release of sICAM‐1.ObjectiveWe wondered whether cetirizine might influence the release of interleukin‐8 (IL‐8) from human epithelial cells activated with agonists distinct from histamine.MethodsWe used the human lung epithelial cell line A549 for our in vitro studies. IL‐8 release was determined by IL‐8 enzyme immunoassay, the intracellular staining for IL‐8 and NF‐kB was analysed by FACS analysis and IL‐8 mRNA steady state level was studied by Northern blot analysis. Confluent epithelial cell monolayer were pre‐incubated with cetirizine (0.01 −1.0 μmol/L) for 30 min and afterwards activated with pro‐inflammatory cytokines (TNF‐α IL‐1β, IL‐6, IFN‐γ) or different agonists (PMA, NaF, respiratory syncytial virus [RSV]) for 24 h.ResultsEpithelial cells stimulated with TNF‐α IL‐1β, PMA and RSV, respectively, showed a significantly increased release of IL‐8. Pre‐incubation with cetirizine diminished the IL‐8 release from cells activated with TNF‐α or PMA in a significant manner. The reduced IL‐8 release coincided with a diminished percentage of cells expressing IL‐8. Northern blot analysis revealed a reduced steady state level of IL‐8 mRNA in cells pretreated with cetirizine and stimulated with TNF‐α. Furthermore, a decreased amount of accessible DNA‐binding sites of the nuclear factor kappa B (NF‐kB) was determined by FACS analysis.ConclusionsThese results suggest that cetirizine reduced the release of IL‐8 from A549 cells stimulated with PMA and TNF‐α, respectively, by lowering IL‐8 gene expression. Therefore, cetirizine might exert anti‐inflammatory effects beyond its H1‐receptor antagonistic activity in the course of inflammatory respiratory tract disorders such as bronchial asthma and allergic rhinitis.
QT interval monitoring during clinical studies with mizolastine, a new H1 antihistamine
Authors: Delauche‐Cavallier M. C. , Chaufour S. , Guérault E. , Lacroux A. , Murrieta M. , Wajman A. 
Published: March 2003

BackgroundSome H1 antihistamines are at risk for rare but severe dysrhythmias due to an effect on the ventricular repolarization.ObjectiveTo present an overview of the QT interval monitoring performed during the clinical development of mizolastine, a new selective second‐generation H1 antihistamine.MethodsThe ECGs database analysis of clinical studies conducted in volunteers and patients is summarized and focused on the results of reported studies and studies specifically designed for the assessment of the effect of mizolastine on cardiac repolarization, through the QT interval measurements. Mizolastine was orally administered up to 75 mg single dose and 40 mg repeated dose in healthy volunteers (i.e. 7.5 and 4 times the recommended dose, respectively) and at a dose of 10 or 15 mg in patients.ResultsIn healthy volunteers, no increased incidence of QTc values >440 msec or ΔQTc ≥40 msec were recorded compared to placebo. No dose‐related increase in QTc interval was observed. The ECG parameters were not modified by the co‐administration of mizolastine with digoxin, diltiazem and erythromycin, when compared to the effect of each co‐administered drug alone. In patients, the mean QTc interval changes from baseline did not significantly differ from placebo. In comparative studies vs. loratadine a similar incidence of out of range values was observed with mizolastine and loratadine.ConclusionECG monitoring of volunteers and patients included in clinical studies conducted with mizolastine showed no significant effect of mizolastine on cardiac repolarization.
Bronchoprotective effects of atrial natriuretic peptide against propranolol‐induced bronchoconstriction after allergic reaction in guinea pigs
Authors: Mizuguchi  , Myo  , Fujimura  
Published: March 2003

ObjectiveTo study the effects of intravenous atrial natriuretic peptide (ANP) on antigen‐induced bronchoconstriction, propranolol‐induced bronchoconstriction (PIB) after antigen challenge, and histamine‐induced bronchoconstriction in guinea pigs.MethodsAllergic bronchoconstriction was evoked by inhalation of ovalbumin (OA) and PIB was caused when 10 mg/mL of propranolol was inhaled 20 min after OA challenge in passively sensitized and artificially ventilated guinea pigs. 25, 50, 100 and 200 μg/mL of histamine were inhaled for 20 s at 5‐min intervals in non‐sensitized guinea pigs.ResultsPretreatment with ANP in doses of 0.1 and 1.0 nmol/kginjected intravenously 15 min after antigen challenge reduced PIB in a dose‐dependent manner, and 5 min before antigen challenge significantly attenuated PIB but not antigen‐induced bronchoconstriction. Intravenous ANP significantly reduced bronchial responses to increasing concentrations of inhaled histamine in a dose‐dependent manner.ConclusionThese results suggest that ANP possesses protective effects against propranolol‐induced and histamine‐induced bronchoconstriction, albeit by a non‐specific mechanism in guinea pig in vivo.
Allergic sensitization and clinical reactions to latex, food and pollen in adult patients
Authors: Levy  , Mounedji  , Noirot  , Leynadier  
Published: March 2003

BackgroundMany latex‐allergic patients are sensitized to one or more foods. Patients allergic to tree and/or grass pollens are also often sensitized to plant‐derived foods. Atopy, defined in most studies as sensitivity to an aeroallergen, is a risk factor for latex allergy. The relative importance of pollen sensitivity, a sign of atopy, as a risk factor for food allergy in latex‐allergic patients has not, however, been examined.ObjectiveTo investigate the relationship between pollen sensitivity and sensitivity to food in latex‐allergic patients.MethodsForty‐four latex‐allergic patients (Groups 1 and 2), 24 of whom were also allergic to tree and/or grass pollen (Group 1) and 25 pollinosis patients who were not allergic to latex (Group 3) were studied. We obtained a history of reactions to food and skin tested them with 12 fresh‐frozen fruits.ResultsAll 12 foods induced a skin test reaction in at least one patient in each of the three Groups. There were, however, twice as many positive skin test reactions to food in patients with pollinosis, whether or not they were allergic to latex, as there were in patients allergic to latex but not to pollen. Latex‐allergic patients were most likely to have a positive skin test and a history of a reaction to avocado or banana whereas patients with pollinosis only were most likely to have a positive skin test and a history of a reaction to apple, peach or celery.ConclusionsThese results suggest that concomitant allergy to pollen is an important risk factor in determining which plant‐derived foods sensitize latex‐allergic patients.
Evidence to suggest that the phosphodiesterase 4 isoenzyme is present and involved in the proliferation of umbilical cord blood mononuclear cells
Authors: Banner  , Dimitriou  , Kinali  , Page  , Greenough  
Published: March 2003

BackgroundThe type 4 phosphodiesterase (PDE) isoenzyme is the main isoenzyme of PDE involved in the control of adult mononuclear cell proliferation.ObjectiveTo establish whether PDE isoenzymes are present in umbilical cord blood mononuclear cells by the use of selective PDE inhibitors, and to identify which PDE isoenzymes are involved in controlling the proliferation of cord blood mononuclear cells.MethodsCord blood was obtained from normal deliveries and mononuclear cells isolated as described previously [ 1] with some modifications. Mononuclear cells were then stimulated to proliferate with phytohaemagglutinin (PHA) (2 μg/mL) in the presence of selective PDE inhibitors. Proliferation was measured by [3H]‐thymidine incorporation.ResultsThe type 4 PDE inhibitors (CDP840, rolipram and RO 20‐1724), and the mixed PDE3/4 inhibitor, zardaverine, produced a concentration‐related inhibition of PHA‐stimulated cord blood mononuclear cell proliferation (P < 0.05,
anova). The non‐selective PDE inhibitor, theophylline, also produced a concentration‐related inhibition of proliferation (P < 0.05,
anova). In contrast, the PDE1 inhibitor, vinpocetine, the PDE3 inhibitor, siguazodan, and the PDE5 inhibitor, zaprinast, were unable to inhibit cord blood mononuclear cell proliferation.ConclusionPDE4 is present in umbilical cord mononuclear cells and is involved in the control of cord blood mononuclear cell proliferation.
Sensitization to inhaled antigen by intratracheal instillation of dendritic cells
Authors: Lambrecht  , Peleman  , Bullock  , Pauwels  
Published: March 2003

BackgroundAirway dendritic cells (DCs) capture and present inhaled antigen. It is not known whether antigen presentation by DCs in the airways is sufficient to induce sensitization to inhaled antigen in vivo.MethodsRats were immunized by intratracheal instillation of ovalbumin (OVA) ‐pulsed bone marrow‐derived DCs or macrophages and exposed 10 days later to a 30‐min aerosol of OVA on 3 consecutive days. Total and differential cell counts and flow cytometry on bronchoalveolar lavage (BAL) fluid, airway histology and serum OVA‐immunoglobulin (Ig) E levels were analysed 24 h after the last exposure.ResultsAs few as 2 × 104 OVA‐DC induced sensitization to inhaled OVA. The secondary response to OVA‐aerosol consisted of an antigen‐specific increase in the number of bronchoalveolar mononuclear cells, activated CD4‐positive αβ‐TCR T lymphocytes, neutrophils and few eosinophils. Peribronchial and perivascular mononuclear cell infiltrates were seen on histological analysis. There was no production of systemic OVA‐IgE. Bone marrow‐derived macrophages did not induce sensitization.ConclusionDelivering antigen to the respiratory tract via professional antigen‐presenting DCs sensitizes for a secondary response to inhaled antigen leading to airway inflammation. This model will prove very useful for studying the early events of sensitization to inhaled antigen using the respiratory route.