bluuebunny/crossref_metadata_2025_split huggingface dataset:
A randomized trial of dehumidification in the control of house dust mite
Authors: Hyndman  , Vickers  , Htut  , Maunder  , Peock  , Higenbottam  
Published: March 2003

BackgroundHouse dust mites (HDM) are sensitive to humidity. Few studies have adequately examined the potential of dehumidification in reducing HDM numbers.ObjectiveThe study examined the effect of portable domestic dehumidifiers, and a behavioural programme to reduce humidity, on HDM counts and HDM allergen levels.MethodsA randomized controlled trial was undertaken. A total of 76 homes were allocated to three groups that received a portable domestic dehumidifier, a behavioural programme, or no intervention. Humidity, temperature, HDM counts (trap and vacuum samples), HDM allergen, and other details of the home environment were measured on four occasions over a period of 1 year. Interventions and measurements were concerned predominantly with one bedroom.ResultsThere was a reduction in relative humidity in the dehumidifier group, but not the behavioural group. A decline in HDM trap counts was observed for all three groups. Change scores did not indicate that the dehumidifier group had a greater decline than the other groups. A secondary analysis examining presence or absence of HDM showed a shift from households having HDM at baseline to households not having HDM in the final round for some trap measures. Change score analysis indicated that this shift was greater in the dehumidifier group compared with other groups. The dehumidifier group did not show a greater decline in HDM allergen than that seen in the other two groups.ConclusionNeither the dehumidifier nor the behavioural intervention had a major effect on HDM counts or allergen levels. However, the study did have a number of limitations relating to size, timing of intervention, and running of the dehumidifiers. The secondary data analysis may indicate some effect of dehumidification, but clearly this effect was small. There is a need for more information on the effects of reducing ambient humidity on the distribution of HDM within their habitats.
Localization of a major allergen, Der p 2, in the gut and faecal pellets of Dermatophagoides pteronyssinus
Authors: Park  , Lee  , Lee  , Ree  , Kim  , Hong  , Yong  
Published: March 2003

BackgroundThe house dust mite Dermatophagoides ptronyssinus is one of the most significant indoor sensitizing agents of allergy. Allergen localization may indicate the importance of secreted materials, faeces, and nonexcreted mite body components as allergen sources.ObjectiveThis study attempted to localize the sites and concentrations of Der p 2 in the cryostat sections of D. pteronyssinus using antirecombinant Der p 2 monoclonal antibody.MethodsMale and female mites and mite faeces collected separately from both sexes were used. Live mites were embedded and serial cryostat sections for light microscopy were performed. Anti‐recombinant Der p 2 monoclonal antibody previously produced by the authors was used. For immunoprobing, mite cryostat sections were incubated in the following antibody‐containing solutions: monoclonal antibody against Der p 2 was initially applied to the sections and fluorescent isothiocyanate conjugated antimouse immunoglobulin G was reacted as the secondary antibody. The faecal pellets were treated the same as described above.ResultsImmunofluorescent probing of cryostat sections with the monoclonal antibody showed labelling of the gut lining, gut contents and defecated faecal pellets. No other internal organs were identified as positively labelled.ConclusionThis study suggested that a major allergen, Der p 2, found in the house dust mite D. pteronyssinus is derived from the digestive tract and concentrated in the faeces.
Regulation of cyclooxygenase‐1 and ‐2 expression in human nasal mucosa. Effects of cytokines and dexamethasone
Authors: Fernández‐Morata  , Mullol  , Fuentes  , Pujols  , Roca‐Ferrer  , Pérez  , Xaubet  , Picado  
Published: March 2003

BackgroundCyclooxygenase (COX) converts arachidonic acid in prostanoids. COX exists in two isoforms, COX‐1 is the constitutive whereas COX‐2 is the inducible isoform. The regulation of COX‐1 and COX‐2 expression in nasal mucosa has not been previously reported.AimWe studied expression and regulation by cytokines and corticosteroids of COX‐1 and COX‐2 in human nasal mucosa. Cultured human nasal explants from patients undergoing corrective nasal mucosal resection were examined for COX‐1 and COX‐2 expression by semiquantitative competitive PCR and Western blot.MethodsExplants were incubated with pro‐(IFNγ, IL‐1β, and TNF‐α) and anti(IL‐10) inflammatory cytokines and dexamethasone. The mechanisms which regulate COX‐2 mRNA expression were studied using inhibitors of translation (Actinomycin D) and transcription (Cicloheximide).ResultsThe baseline expression of COX‐2 mRNA was higher than COX‐1 mRNA. Once in culture, there was a slight spontaneous up‐regulation of COX‐1 and a strong COX‐2 mRNA and protein up‐regulation. The incubation of nasal explants with pro‐inflammatory cytokines increased the expression of COX‐2 mRNA and protein, from 1 to 24 h of incubation in a dose‐related manner. The regulation of these effects occurred at both transcriptional and post‐transcriptional levels. Dexamethasone and IL‐10 abrogated cytokine‐induced COX‐2 mRNA and protein expression. Pro‐inflammatory cytokines, dexamethasone and IL‐10 had no effect on COX‐1 mRNA expression.ConclusionsAs prostanoids have important regulatory effects on the immunologically mediated inflammatory responses, our findings throw some light on the mechanisms that regulate the enzymes which produce these metabolites in the human airway.
Cytokine responses to Der p 1 and Der p 7: house dust mite allergens with different IgE‐binding activities
Authors: Hales  , Shen  , Thomas  
Published: March 2003

BackgroundThere is very limited information comparing T‐cell responses to different house dust mite (HDM) allergens even though T cells are essential in the initiation and regulation of immunoglobulin (Ig) E synthesis and eosinophilia.ObjectiveTo compare the level of T‐cell proliferation and cytokine production to the group 1 and group 7 HDM allergens which are known to have different IgE‐binding capabilities.MethodsFreshly isolated peripheral blood mononuclear cells (PBMC) from HDM‐allergic and HDM‐nonallergic donors were stimulated with the group 1 and group 7 allergens of Dermatophagoides pteronyssinus and the level of proliferation as well as IL‐5 and IFNγ production were measured.ResultsThe proliferative and IL‐5 production to the group 1 and group 7 allergens were equivalent despite the group 7 allergen's lower frequency of IgE‐binding. However more IFNγ was produced to Der p 7 than to Der p 1, particularly for the nonallergic donors. As expected IL‐5 production was much higher for PBMC from the allergic donors than for cells from nonallergics; however, there was no difference in the level of T‐cell proliferation between the donor groups.ConclusionThe relative importance of the individual HDM allergens is normally determined by measuring the frequency of IgE‐binding to the allergen in sera from an allergic population. The equivalent increased IL‐5 response of PBMC from allergic people to the group 1 and group 7 allergens despite the different IgE‐inducing activity indicates that these allergens may be equally capable of contributing to an asthmatic response by inducing eosinophilia.
Expression of platelet‐derived endothelial cell growth factor and vascularity in the nasal mucosa from allergic rhinitis
Authors: Mori S. , Fujieda S. , Sunaga H. , Fox S. B. , Saito H. 
Published: March 2003

BackgroundAngiogenesis plays critical roles in various pathological mechanisms. It has been hypothesized that the vascularity in allergic nasal mucosa is different from that in normal mucosa, and that changes in the vascular network contributes the pathogenesis of allergic rhinitis.ObjectiveTo determine whether hypervascularity and overexpression of the platelet‐derived endothelial cell growth factor (PD‐ECGF), an angiogenic factor, are found in allergic nasal mucosa and whether these two factors are associated with the allergic reaction.MethodsWe investigated the expression of PD‐ECGF and counted microvessels in 51 nasal mucosae (30 samples from patients with allergic rhinitis and 21 samples as control from normal subjects) using an immunohistochemical technique.ResultsPD‐ECGF expression in allergic nasal mucosae was significantly higher than that in control mucosae at the interstitium of the lamina propria (P = 0.0024) and nasal gland (P = 0.024). PD‐ECGF positive areas were coincident with areas of high vascularity in the sections. The microvessel count in the lamina propria of allergic mucosae was higher than that of control mucosae (P = 0.050). Regarding the correlation with various clinical factors, the total nasal symptom score was significantly associated with both the PD‐ECGF expression in the interstitium of the lamina propria (P < 0.05) and in the nasal gland (P < 0.005), as well as with the number of vessels (P < 0.05).ConclusionPD‐ECGF and hypervascularity in the nasal mucosa may be involved in the pathogenesis of allergic rhinitis.
Airway inflammation in a murine model of chronic asthma: evidence for a local humoral immune response
Authors: Kumar R. K. , Temelkovski J. , Mcneil H. P. , Hunter N. 
Published: March 2003

BackgroundAsthma is an acute‐on‐chronic inflammatory disease of the airways characterized by recruitment of eosinophils into the epithelial layer, chronic inflammation in the lamina propria, as well as variable accumulation of mast cells in the airway wall. The role of local production of allergen‐specific immunoglobulins in triggering mast cell‐mediated asthmatic inflammation is unknown.MethodsWe used a chronic inhalational exposure model of asthma in ovalbumin‐sensitized BALB/c mice to examine the phenotype of immunoglobulin‐secreting cells and mast cells in the airway wall. In parallel, we assayed ovalbumin‐specific IgG and total IgE in the plasma of these animals.ResultsIn sensitized mice exposed to aerosolized ovalbumin for 6 weeks, aggregates of chronic inflammatory cells consisted of a majority of plasmacytoid cells, including numerous IgG‐synthesizing cells, which were significantly increased in sensitized animals compared to controls. IgA‐synthesizing cells were also present, but were not increased in the sensitized exposed mice. Immunoglobulins in the cytoplasm of the plasma cells were demonstrated to be antigen‐specific. No IgM‐or IgE‐synthesizing cells were observed, although levels of total IgE in the plasma were significantly increased. There was no recruitment of mast cells of either the mucosal or the connective tissue phenotype into the lamina propria or the epithelium.ConclusionIn this experimental model of chronic asthma, the pattern of inflammation in the airway wall is consistent with development of a local IgG‐mediated humoral immune response. However, there is no evidence of local production of IgE or recruitment of mast cells.
Upregulation of nasal mucosal eotaxin in patients with allergic rhinitis during grass pollen season: effect of a local glucocorticoid
Authors: Pullerits T. , LindÉn A. , Praks L. , Cardell L. O. , LÖtvall J. 
Published: March 2003

BackgroundAllergic rhinitis is a common disease characterized by infiltration of eosinophils into the nasal mucosa during the periods of symptoms. Among chemokines, which attract cells to the site of inflammation, eotaxin is relatively specific for eosinophils.ObjectiveWe examined the influence of grass pollen season on nasal eotaxin expression in patients with seasonal allergic rhinitis, as well as the effect of a nasal glucocorticoid on this eotaxin expression.MethodsNineteen patients with allergic rhinitis received treatment with either nasal beclomethasone (400 μg/day) or placebo over a grass pollen season. In these patients, nasal biopsies were taken prior to and during the peak of the pollen season and stained immunohistochemically for eotaxin and EG2 + eosinophils. Five healthy subjects served as controls and gave nasal biopsies once prior to the pollen season.ResultsPrior to pollen season, there was no significant difference in nasal eotaxin expression between patients with allergic rhinitis and healthy subjects. Grass pollen season induced significant increase in eotaxin expression in placebo‐treated (P = 0.04; n = 9) but not in beclomethasone‐treated rhinitis patients (P = 0.8; n = 10). During peak grass pollen season, the eotaxin expression in placebo‐treated patients was significantly higher compared with healthy subjects outside season (P = 0.03). There was no significant correlation between the expression of eotaxin and the number of EG2 + eosinophils in nasal mucosa. The serum levels of eotaxin in rhinitis patients remained stable over the pollen season.ConclusionExpression of eotaxin in nasal mucosa of grass‐pollen allergic rhinitis patients is upregulated during pollen season and treatment with a nasal glucocorticoid protects against this upregulation.
Immunological and molecular characterization of the major allergens from lilac and privet pollens overproduced in Pichia pastoris
Authors: González E. , Villalba M. , Rodríguez R. 
Published: March 2003

The main allergens from privet and lilac pollens, Lig v 1 and Syr v 1, are proteins homologous to Ole e 1 and have been shown to be involved in cross‐reactivity.To overproduce the correctly folded Lig v 1 and Syr v 1 allergens and to study their immunological properties in comparison with those of their natural counterparts.The yeast Pichia pastoris was used as an expression system to produce these recombinant allergens. The proteins were isolated by ion‐exchange and size‐exclusion chromatographies. Amino acid quantifying, Edman degradation, mass spectrometry and circular dichroism were carried out to obtain molecular properties of the recombinant proteins. Anti‐Ole e 1 monoclonal and polyclonal antibodies, as well as sera from patients allergic to olive pollen, were used in immunoblotting and ELISA for immunological characterization.Recombinant Lig v 1 and Syr v 1 were secreted at high yield to the extracellular medium of the yeast. The purified proteins displayed the native conformation, as deduced from their spectroscopic properties and binding ability to an IgG monoclonal antibody. The recombinant allergens behaved similarly to their natural counterparts when they were analysed against Ole e 1‐specific antibodies. IgE and IgG binding properties of lilac and privet allergens to olive allergic sera and Ole e 1‐specific antibodies indicated that these molecules share common B‐cell epitopes with Ole e 1. P. pastoris yeast is an appropriate system for the efficient production of Ole e 1‐like allergens, which could be used as analogous allergens and predictors of clinical sensitization.
Effect of a specific cysteinyl leukotriene‐receptor 1‐antagonist (montelukast) on the transmigration of eosinophils across human umbilical vein endothelial cells
Authors: Virchow Jr J. C. , Faehndrich S. , Nassenstein C. , Bock S. , Matthys H. , Luttmann W. 
Published: March 2003

Background Leukotrienes have been implicated in the selective infiltration of eosinophils into the bronchial mucosa in asthma.Objective We studied whether eosinophil transmigration through cultured human umbilical vein endothelial cells (HUVECs) can be blocked by a specific cysteinyl LT1‐receptor‐antagonist.Methods Unstimulated and stimulated eosinophils from patients with asthma and normal controls were subjected to confluent human umbilical vein endothelial cell (HUVEC) monolayers separating the upper and lower chamber of Transwell™‐culture plates. Unstimulated eosinophils or cells pre‐incubated in the presence of the eosinophil activating cytokines GM‐CSF or IL‐13 were placed in the upper chambers while PAF, a potent chemoattractant factor for eosinophils, was added to the lower chamber. Migration of eosinophils was quantified by a β‐glucuronidase assay.Results The assumption that eosinophils express CysLT1 (cysteinyl‐leukotriene 1)‐receptors was based on our demonstration of mRNA‐expression for the CysLT‐1‐receptor by polymerase chain reaction on purified eosinophils. The chemotactic response to PAF was significantly reduced when eosinophils were pre‐incubated with montelukast for 15 min. When eosinophils were pre‐incubated with GM‐CSF and/or IL‐13, the migratory response to PAF was also significantly reduced by montelukast.Conclusion From these data we conclude that the specific cysteinyl LT1‐receptor antagonist montelukast can inhibit PAF‐induced eosinophil transmigration through cultured HUVEC monolayers.
Fusarium solani major allergen peptide IV‐1 binds IgE but does not release histamine
Authors: Verma J. , Sridhara S. , Singh B. P. , Pasha S. , Gangal S. V. , Arora N. 
Published: March 2003

Background Fusarium solani (FS) is an important allergen source afflicting 4% of the nasobronchial allergy patients. Fus s I3596*, a 65 kDa major glycoprotein allergen of FS reacts with 95% fungus sensitive patients.Objectives To purify and characterize a potent peptide from Fus s I3596* which may be useful for therapeutic purposes.Methods The 65 kDa protein was sequentially cleaved with trypsin and cyanogen bromide (CNBr). The cleaved products were purified on reverse phase high performance liquid chromatography (rpHPLC) column and functionally characterized by in vitro and in vivo methods for its IgE binding and histamine release.Results The protein on cleavage showed 11 peaks (I to XI). Of these, peaks I, III, IV and V were highly allergenic as determined by IgE ELISA. These peaks were further purified and peptide IV‐1 was most potent in comparison to other peptides by ELISA‐inhibition. This peptide showed IgE binding but could not evoke intradermal response in Fusarium‐sensitive patients. Heparinized blood challenged with peptide IV‐1 does not release histamine. Preincubation of heparinized blood with peptide IV‐1 and challenging with crude extract blocked histamine release in a dose dependent manner.Conclusion Peptide IV‐1 binds to IgE but does not release histamine, demonstrating its potential use in therapy of Fusarium‐allergic patients.
IgE‐dependent release of myeloperoxidase by neutrophils from allergic patients
Authors: Monteseirín J. , Bonilla I. , Camacho M. J. , Conde J. , Sobrino F. 
Published: March 2003

Background The three forms of IgE receptor: the heterotrimeric high‐affinity receptor for IgE (FcεRI), the low‐affinity receptor for IgE (FcεRII/CD23) and the Mac‐2/IgE‐binding protein (εBP), have previously been found on human neutrophils. We have previously shown that specific allergens are able to activate functional responses by neutrophils from allergic patients sensitized to those allergens. Neutrophils are present in the sites of allergic inflammation. The primary (azurophilic) granules of neutrophils contain a variety of enzymes that might potentiate inflammation, such as myeloperoxidase (MPO). It is not known whether specific allergens are able to elicit MPO release by neutrophils from allergic patients.Methods Neutrophils were challenged in vitro with the specific allergen that produced clinical symptoms in asthmatic patients. Also, the cells were challenged with allergens that the patients were not sensitive to. Neutrophils from normal subjects were also challenged with allergens.Results The in vitro challenge of neutrophils with allergens that the patients were sensitive to elicited a release of MPO by these cells. The in vitro activation of neutrophils was highly allergen‐specific, in such a way that allergens other than those accounting for clinical symptoms did not evoke MPO release, and allergens were ineffective on neutrophils from healthy donors.Conclusion An IgE‐dependent mechanism might promote MPO release by neutrophils at allergic sites.
In vivo airway eosinophil accumulation induced by polymyxin‐B reduces bronchial responsiveness in guinea pigs
Authors: Ishiura Y. , Fujimura M. , Myou S. , Nobata K. , Liu Q. , Yamamori C. , Amemiya T. 
Published: March 2003

Background Chronic desquamative eosinophilic bronchitis and bronchial hyperresponsiveness have been considered essential for bronchial asthma. However, it has not been studied whether airway eosinophils enhance or inhibit bronchial responsiveness in vivo.Objective This study was conducted to elucidate the influence of airway eosinophil accumulation on bronchial responsiveness in vivo.Materials and methods Guinea pigs were transnasally treated with 75 µg/kg of polymyxin‐B or vehicle twice a week for a total of 3 weeks. Guinea pigs were surgically cannulated and artificially ventilated 24 h after the last administration of polymyxin‐B or vehicle. Ten minutes after the installation of artificial ventilation, ascending doses of methacholine, acetylcholine or histamine were inhaled for 20 s at intervals of 5 min. Subsequent study was conducted 20 min after treatment of 60 mg/kg of indomethacin in the same manner. Final study was conducted in naive guinea pigs after single inhalation of 75 µg/mL of polymyxin B.Results The proportion of eosinophils in bronchoalveolar lavage fluid significantly increased in guinea pigs treated with polymyxin‐B compared with vehicle. Bronchial responsiveness to inhaled methacholine, acetylcholine and histamine was significantly decreased by the polymyxin‐B treatment. This protective effect induced by polymyxin B was abolished by pretreatment of indomethacin. A significant increase in bronchial responsiveness was observed after a single inhalation of polymyxin B.Conclusion These results suggest that in vivo airway eosinophils may reduce non‐specific bronchial responsiveness through inhibitory or bronchoprotective prostanoids.
IgE binding components in Tetranychus urticae and Panonychus ulmi‐derived crude extracts and their cross‐reactivity with domestic mites
Authors: Kim Y.‐K. , Oh S.‐Y. , Jung J.‐W. , Min K.‐U. , Kim Y.‐Y. , Cho S.‐H. 
Published: March 2003

Background Recent investigation has revealed that spider mites such as Tetranychus urticae and Panonychus ulmi are important allergens in the development of occupational asthma among apple farmers.Objective To evaluate IgE binding components in T. urticae and P. ulmi‐derived crude extracts and their cross‐reactivity with Panonychus citri, Tyrophagus putrescentiae and Dermatophagoides pteronyssinus in apple cultivating farmers.Methods Thirty‐one apple farmers with positive skin responses to T. urticae or P. ulmi were randomly recruited, and specific IgE levels in their sera were measured using ELISA. Cross‐reactivity was evaluated by ELISA inhibition. IgE binding components were evaluated by IgE immunoblotting.Results A total of 11 IgE binding components in T. urticae and 10 in P. ulmi were found. Among them, the 17 kDa, 27 kDa, 33 kDa, 37 kDa, 41 kDa, 56 kDa, and 75 kDa allergens in T. urticae, and the 33 kDa, 41 kDa, and 51 kDa allergens in P. ulmi were identified as dominant allergens. T. urticae‐specific IgE binding was completely inhibited by 100 μg/mL of T. urticae (99.7%), but only partially inhibited by P. citri (83.0%), P. ulmi (71.6%), T. putrescentiae (69.7%), and D. pternonyssinus (60.1%). P. ulmi‐specific IgE binding was completely inhibited by additions of P. citri (92.3%) and P. ulmi (91.2%), but only partially inhibited by the addition of T. urticae (61.5%), T. putrescentiae (57.7%), and D. pteronyssinus (54.4%).Conclusion There were seven dominant allergens found in T. urticae and three in P. ulmi. T. urticae‐ and P. ulmi‐specific IgE bindings were partially inhibited by crude extracts derived from D. pteronyssinus and T. putrescentiae.