bluuebunny/crossref_metadata_2025_split huggingface dataset:
A double‐blind, placebo‐controlled trial of local nasal immunotherapy in allergic rhinitis to Parietaria pollen
Authors: D'AMATO G. , LOBEFALO G. , LICCARDI G. , CAZZOLA M. 
Published: April 2006

SummaryWe assessed the efficacy and safety of local nasal immunotherapy (LNIT) using an extract in macronized powder form of Parietaria pollen, a very important allergenic plant in the Mediterranean and other parts of the world. Twenty‐six patients aged 13–37 years, with seasonal allergic rhinitis to this pollen, were enrolled in a double‐blind placebo‐controlled trial, carried out from autumn 1991 to the end of June 1992. They were selected on the basis of a positive skin‐prick test, radioallergosorbent test (RAST) and intranasal challenge to Parietaria antigen. Patients were randomly divided into two groups of 13; the first group was given Parietaria antigen, and the second placebo. We recorded mean weekly symptom scores and drug consumption for 17 weeks during the pollen season in the year 1992, and specific serum‐IgE and IgG levels. Three patients in the active group withdrew from the study because of bronchial symptoms. A significant difference was observed in mean weekly nasal symptom scores, in drug consumption and in specific nasal threshold to Parietaria allergenic extract in the treated and control groups. No difference was observed in serum IgE and IgG levels. Serum IgE levels rose significantly only in the control group after the pollen season. This study indicates that LNIT may be a useful alternative to traditional subcutaneous immunotherapy in patients with allergic rhinitis.
Epithelial pathways for luminal entry of bulk plasma
Authors: ERJEFÄLT J. S. , ERJEFÄLT I. , SUNDLER F. , PERSSON C. G. A. 
Published: April 2006

SummaryInflammatory challenges of the airway mucosa cause luminal entry of bulk plasma. Extravasation of plasma is well described but the routes for epithelial passage of plasma are largely unknown. Using colloidal gold (5 nm) as tracer we have now examined the fate of extravasated plasma in the airways. The tracer was given intravenously to anaesthetized, ovalbumin‐sensitized guinea‐pigs 2min prior to airway mucosal challenge with 12pmol ovalbumin (the dose was selected from a separate dose‐response study). Tissue specimens were collected 30s, 3 and 6 min after end of challenge (separate time course experiments suggested that the peak rate of entry of plasma occurred at about 5 min). The colloidal gold particles were visualized by autometallographic silver intensification. The gold produced no circulatory disturbance and had a uniform vascular distribution with negligible adherence to vascular endothelium. After challenge gold was first widely distributed in the lamina propria. At 3 and 6 min the tracer was also in the epithelium and airway lumen. It appeared that plasma was moved distinctly between and all around each epithelial cell. Bright field‐, scanning‐, and transmission electron‐microscopy indicated that the luminal entry of plasma did not affect the integrity of the epithelial lining. This study demonstrates that the plasma exudate moves across an intact epithelial layer through ubiquitous paracellular pathways. Even at a pronounced acute plasma exudation response exceedingly small amounts of plasma may pass around a single cell explaining the non‐injurious nature of mucosal exudation of bulk plasma in health and disease.
House dust mite allergen levels in two cities in Canada: effects of season, humidity, city and home characteristics
Authors: CHAN‐YEUNG M. , BECKER A. , LAM J. , DIMICH‐WARD H. , FERGUSON A. , WARREN P. , SIMONS E. , BRODER I. , MANFREDA J. 
Published: April 2006

SummaryThe homes of 120 patients with asthma, 57 in Vancouver and 63 in Winnipeg, were studied. The characteristics of the homes were assessed by a questionnaire. Dust samples were collected and the indoor relative humidity was measured four times during the year covering all four seasons in both cities. Mite allergen levels were determined using monoclonal antibodies against Der p I and Der f I by the ELISA method. The mean levels of both mite allergens in mattress and floor samples in the homes in Vancouver and in Winnipeg were relatively low for all seasons. Mite allergen levels were found to be associated with city, season and individual home differences. They were significantly higher in Vancouver than in Winnipeg. Der p I and Der f I in mattress samples in both cities and Der f I in floor samples in Vancouver, varied by season. The indoor relative humidity level in the homes in Vancouver were also significantly higher than those in Winnipeg. There was, however, no significant association between the levels of indoor relative humidity and the levels of mite allergens after adjusting for variations in city, season and individual home. Although individual home differences were highly associated with mite allergen levels, only a few home characteristics were found to be related to mite allergen levels such as the type and the age of the home, the type of heating, the use of feather pillows and the number of occupants in the homes. Whether low levels of mite allergens are partially responsible for the relatively low prevalence of childhood asthma in Canada remains to be investigated.
A standardized densitometric immunoblotting analysis of Candida albicans protein allergens
Authors: SAVOLAINEN J. 
Published: April 2006

SummarySera from 196 patients with a strong skin reactivity to Candida albicans and a history of atopic disease were used for C. albicans IgE‐immunoblotting. The IgE‐immunoblots were analysed by densitometry and integration of the densitogram peaks. A standardized reference disc system allowed parallel analysis of several different immunoblotting experiments. Altogether 105 patients had C. albcans specific IgE antibodies in immunoblotting. The IgE‐response against C. albicans was extremely polyspecific and was directed against 42 different bands. The most important IgE binding bands were 46 kDa and 27 kDa bands against which 44 (42%) and 29 (28%) patients, respectively, had IgE responses. A combination of IgE‐immunoblotting and densitometry was found practical in analysis of large number of patient sera allowing a profound and accurate analysis and characterization of C. albicans allergen extract. This data evolved from a sufficiently large patient population can be utilized in further standardization of C. albicans extracts.
Antiallergic activity of loratadine: inhibition of leukotriene C4 release from human leucocytes
Authors: MIADONNA A. , MILAZZO N. , LORINI M. , MARCHESI E. , TEDESCHI A. 
Published: April 2006

SummaryThe H1 antagonist loratadine has the capacity to inhibit histamine release from human basophils. The aim of this study was to investigate whether loratadine can also inhibit leukotriene C4 (LTC4) release from human leucocytes. Basophil‐enriched mononuclear cell suspensions were prepared by centrifugation of peripheral venous blood (n= 10) on discontinuous Percoll gradients. Leucocytes were stimulated with anti‐IgE, N‐formylmethionyl‐leucyl‐phenylalanine (FMLP) and Ca2+ ionophore A23187; immunoreactive (i) LTC4 release in the cell supernatant was measured by a competitive radioimmunoassay and histamine release was evaluated by an automated fluorometric technique. Loratadine, in the concentration range of 1–50μM, exerted a dose‐dependent inhibitory effect on IgE‐mediated and IgE‐independent histamine and iLTC4 release. The concentrations inhibiting 50% of histamine release were 30 μM (anti‐IgE), 27μM (FMLP) and 19μM (Ca2+ ionophore A23187). The concentrations inhibiting 50% of iLTC4 release were 2–3 μM (anti‐IgE). 11 μM (FMLP) and 1.7μM (Ca2+ ionophore A23187). The inhibitory activity on iLTC4 release was optimal after preincubation for 2h at 37°C, and was no longer evident when leucocytes were stimulated 2h after cell washing. Increased extracellular Ca2+ concentrations reduced the inhibitory activity of loratadine. These results indicate that loratadine has the capacity to inhibit the release of preformed and newly generated mediators from human basophil‐enriched mononuclear cell suspensions.
Ability of inhaled procaterol, a β32 adrenoceptor agonist, to attenuate eicosanoid‐induced airflow obstruction and airway microvascular leakage
Authors: TOKUYAMA K. , ARAKAWA H. , MOCHIZUKI H. , MORIKAWA A. 
Published: April 2006

SummaryBeta‐2 adrenoceptor agonists are widely used as bronchodilators in the treatment of asthma mainly via inhalation. In the present study, we evaluated the ability of inhaled procaterol, a β2 adrenoceptor agonist, to reduce eicosanoid‐induced airway micro‐vascular leakage, and compared the ability with its inhibitory effect against bron‐choconstriction. Tracheostomized guinea‐pigs were given aerosolized procaterol (10 or 100 μg/ml) for 10min under spontaneous breathing. Immediately after the end of inhalation, the animals were mechanically ventilated. Fourteen minutes after the end of inhalation, Evans blue dye (20mg/kg) was given i.v. One minute later, 2nmol/kg leukotriene D4 (LTD4), 50 nmol/kg U‐46619, a thromboxane A2 mimetic, or vehicle was administered i.v. LTD4‐ or U‐46619‐induced increase in lung resistance was measured for 6 min. After removing the lungs, the amount of extravasated Evans Blue due in the lower airways was examined as an index of microvascular leakage. Inhaled procaterol significantly attenuated increases in both lung resistance and Evans Blue dye extravasation caused by these eicosanoids. The degree of inhibition was almost complete for lung resistance (approximately 90%), but it was only partial (range 18.5–61.2%) for the dye extravasation. No significant changes in mean systemic blood pressure and in heart rate was observed after an inhalation of 10μg/ml procaterol. These results suggest that inhaled β2 adrenoceptor agonists may reduce airway microvascular leakage caused by inflammatory mediators such as eicosanoids without affecting systemic circulation. However, these agonists may attenuate airway microvascular leakage only partially even in doses which can inhibit bronchoconstric‐tion almost completely.
Asthmatic symptoms and indoor levels of micro‐organisms and house dust mites
Authors: BJÖRNSSON E. , NORBÄCK D. , JANSON C. , WIDSTRÖM J. , PALMGREN U. , STRÖM G. , BOMAN G. 
Published: April 2006

SummaryAs a part of a worldwide investigation on the prevalence of respiratory symptoms, we have performed a study on the relationship between the indoor environment and asthma‐like symptoms in the population of a central Swedish municipality. The study comprised 88 individuals, aged 20–45 years who underwent a structured interview, spirometry, a methacholine provocation test, skin‐prick tests and blood samples for measurements of serum concentrations of eosinophil cationic protein (S‐ECP), blood eosinophil count and total immunoglobulin E (S‐IgE). In the homes, the room temperature, air humidity, respirable dust, house dust mites (HDM) and airborne micro‐organisms were measured. The relative humidity in all the homes was found to be above 33%. HDM were found in 13% of homes. In the homes of the 47 subjects with asthma related symptoms, significantly higher total levels of bacteria and mould (P<0.05) and a higher proportion of detected HDM (OR = 5.3) was found than in subjects with no asthma related symptoms, after adjustment for age, sex, smoking, indoor temperature and air humidity. HDM were found to be an independent risk factor for asthma related symptoms (OR = 7.9) and nocturnal breathlessness (OR = 6.2) (P<0.05), while the total level of bacteria was a risk factor for asthma related symptoms and wheezing (P<0.05). We conclude that although HDM is relatively infrequently found in the homes of central‐Sweden, the presence of HDM is related to asthmatic symptoms. A relation between levels of airborne bacteria and asthma related symptoms was also found.
Validation and application of a new simple strategy for measurements of urinary leukotriene E4 in humans
Authors: KUMLIN M. , STENSVAD F. , LARSSON L. , DAHLÉN B. , DAHLEN S.‐E. 
Published: April 2006

SummaryTo monitor endogenous production of cysteinyl‐containing leukotrienes, the end‐metabolite leukotriene E4 (LTE4) was analysed in urine. Results obtained with a sensitive enzyme immunoassay (EIA), performed on crude urine samples correlated well with data obtained from a previously reported radioimmunoassay. Enzyme immunoassay analysis of unextracted urine was justified by an excellent agreement between analyses in crude samples and measurements achieved after purification on solid phase extraction followed by separation on reversed‐phase high performance liquid chromatography. Moreover, LTE4 was stable in urine samples stored at ‐20°C, for months without the addition of preservatives. The stability of LTE4 in urine was not improved by addition of the antioxidant 4‐hydroxy‐TEMPO and pH adjustment to 9. As assessed by EIA analysis in crude urine samples, baseline values for urinary leukotriene E4 were not significantly different between atopic asthmatic subjects and non‐asthmatic individuals, and there was no diurnal variation in urinary excretion of LTE4 in healthy subjects. However, we confirmed earlier data on significantly higher basal levels of urinary LTE4 in aspirin‐intolerant asthmatics. In addition, a post‐challenge increase in urinary LTE4 levels was detected in association with allergeninduced airway obstruction in atopic asthmatics. The per cent increase in urinary LTE4 was similar, irrespective of whether the samples were purified or not prior to EIA. Thus, combined with random validation by high performance liquid chromatography, the strategy of direct EIA of serially diluted urine samples was found to be a good index of in vivo production of leukotrienes. This was further reinforced by the demonstration that pretreatment with the leukotriene biosynthesis inhibitor Bay × 1005 inhibited the post allergen‐challenge increase in urinary LTE4, as shown both with unpurilied and purified samples.
Psychiatry in the allergy clinic: the nature and management of patients with non‐allergic symptoms
Authors: HOWARD L. M. , WESSELY S. 
Published: April 2006

SummaryPatients with multiple unexplained somatic symptoms attributed to allergy frequently present to physicians and often the physician fails to find evidence for allergic or immunological mechanisms underlying the presenting symptoms. This article discusses the social and cultural background to this disorder. We then consider current explanatory models for symptoms and finally, we consider appropriate management, starting with the initial consultation, the identification of psychiatric disorders when present, and concluding with suggestions for subsequent treatment and guidance on appropriate referral.
Characterization of IgE‐binding epitopes on Candida albicans enolase
Authors: ITO K. , ISHIGURO A. , KANBE T. , TANAKA K. , TORH S. 
Published: April 2006

Summary Candida albicans enolase is one of the important allergens in Candida allergy. We isolated and purified 46 kDa C. albicans enolase (CAE) from C. albicans and characterized epitopes for IgE antibody by lectin‐blotting and enzymatic digestion followed by sodium dodecyl sulfale polyacrylamide gel electrophoresis (SDS‐PAGE) and immunobiotting. Lectin blotting and deglycozilation indicated that this protein did not contain polysaccharide side chains. The purified CAE and recombinant fusion protein produced from CAE gene possessed common epitopes for IgE antibody. We estimated IgE binding epitopes on the basis of reported amino acid sequences from the analysis of cDNA encoding CAE. V8 protease digestion of CAE gave six polypeptide fragments (A‐F). The N‐termini of each fragment were confirmed by amino acid sequence and the C‐termini were estimated by molecular weights of each fragment and the specific cutting site of V8 protease. Fragment C (25.0 kDa; F‐171‐I‐399) reacted to 90% IgE antibodies examined, whereas fragments D (21.0 kDa; F‐171‐1‐360), E (16.2kDa: F‐171‐D‐317) and F (13.0kDa; A‐47‐E‐170) showed no IgE binding. Our results suggest that epitopes for IgE antibodies exist near the C‐terminal of the protein.
Differential dependence of TH‐0, TH‐1 and TH‐2 CD4 4+ T cells on co‐stimulatory activity provided by the accessory molecule LFA‐1
Authors: FAITH A. , HIGGINS J. A. , O'HEHIR R. E. , LAMB J. R. 
Published: April 2006

Summary Background The adhesion molecule LFA‐1 contributes to the activation response of peripheral blood human CD4+ T cells. Less is known of its contribution to stimulation of long‐term CD4+ T cell lines and clones or of its potential to co‐stimulate CD4+ T cells of different functional phenotype. Objective This study was therefore performed to investigate co‐stimulatory properties of the LFA‐1 (CD11a/CD 18) complex in the activation of human CD4+ T cell lines and clones of TH‐0. TH‐1 and TH‐2 subsets. Methods Co‐stimulatory activity was measured by cross‐linking antibodies to CD 11a or CD18 with anti‐CD3 antibodies to plastic and then measuring the proliferative response of CD4+ T cells to these antibodies. Results A house duct mite allergen‐specific CD4+ T cell line (TH‐2) demonstrated much greater dependence on both C'DI la and CD IK than a mycobacterial antigen‐specific CD4+ T cell line (TH‐1). Co‐stimulatory activity through LFA‐1 was also provided to a house dust mite‐specific CD4+ T cell clone (DE‐9; TH‐2) but not to an influenza haemagglutinin‐specific CD4+ T cell clone (HA 1.7: TH‐0). In contrast, soluble antibodies to CD 18 inhibited proliferativc responses of both DE‐9 and HA1.7 to an immunogenic challenge of antigen and to stimulation by unti‐CD3 antibodies. However, the allergen‐specific T cells were more susceptible to inhibition. Signal transduction was also observed from the T‐cell receptor to LFA‐1. Ligation of the T‐cell receptor modulated the phenotypic expression of LFA‐1 and ICAM‐1 on both HA1‐7 and DE‐9). Phenotypic modulation was observed as a result of both activation and the induction of non‐responsiveness. Conclusion These experiments indicate that CD4+ T cells of TH‐2 functional phenotype may have a greater requirement for the co‐stimulatory activity of LFA‐1 than CD4+ T cells of TH‐0 or TH‐1 phenotypes.
Regulation of cytokine and chemokine transcription in a human TH2 type T‐cell clone during the induction phase of anergy
Authors: O'HEHIR R. E. , LAKE R. A. , SCHALL T. J. , YSSEL H. , PANAGIOTOPOULOU E. , LAMB J. R. 
Published: April 2006

SummaryBackground
Selected cytokines produced by allergen specific CD4+ T cells from atopic individuals contribute to both the specific and non‐specific effector mechanisms of the allergic itnmune response. The chemokine family of cytokines and tumour necrosis factor (TNF)‐α are leucocyte regulatory and proinflanimatory molecules. The chemokines include interleukin (IL)‐8 and the RANTES/SIS cytokines.Objective
There has been no systematic survey of chemokine production in T‐cell subtypes. Because of their wide range of biological properties, it might be expected that they would be closely regulated by T cells. This paper illustrates one way (through the characterization of T‐cell clones) these questions might be addressed.Methods
Northern blot analysis was used to quantitate steady state transcription of selected cytokine genes and enzyme linked imtiiunosorbent assay (ELISA) was used to quantitate soluble product.Results
mRNA expression of the chemokines (IL‐8, HuMIP‐1α and HuMIP‐1β) and TNFα is upregulated in TH2‐like cloned house dust mite reactive human CD4+ T cells under conditions of activation and during the induction phase of anergy. Although the development of anergy superinduces mRNA for both IL‐8 and TNFα. protein production is low compared with that released during activation. In contrast. RANTES, a chemoattractant for CD4+/CD45RO+ memory T cells, eosinophils and basophils, is constitutively expressed at the RNA level by the T cells and not modulated by signals of activation and anergy induction. The production of IL‐2, IL‐4 and IL‐5 mRNA and proteins during the induction of anergy peaks at 2h after stimulation, whereas the kinetics following activation of the T cells is delayed in comparison.Conclusion
These data show that the induction of the anergic state coincides with post‐transcriptional regulation of selected cytokine genes. Further study of these phenomena will impact on our understanding of the mechanisms of induction of anergy and the regulation of allergic immune responses in desensitization.
Absence of continuous epitopes in the house dust mite major allergens Der p I from Dermatophagoides pteronyssinus and Der f I from Dermatophagoides farinae
Authors: COLLINS S. P. , BALL G. , VONARX E. , HOSKING C. , SHELTON M. , HILL D. , HOWDEN M.E.H. 
Published: April 2006

SummaryBackground
The house dust mite has been shown to be an important source of domestic allergens associated with immediate hypersensitivities. The Group I mite allergens Der p I from Dermatophagoides pteronyssinus and Der f I from D. farinae display extensive amino acid sequence homology and have similarities with cysteine protease enzymes.Objective
The availability of the complete amino acid sequences for these allergens allowed us to search for the allergic detertninants within these molecules. The aim of the present investigation was to identify any continuous IgE‐binding epitopes within these amino acid sequences. We also sought to test the validity of previously reported Der p I peptide epitope sequences.Methods
In order to identity any continuous IgE epitopes, the amino acid sequences of Der p I and Der f I were synthesized as decapeptides overlapping in sequence and coupled to plastic pins. The specific IgE‐binding capacity of these peptides was assayed using an enzyme‐linked biotin‐streptavidin procedure and sera from patients known to be sensitive to these allergens. Previously reported Der p I peptide epitopes were synthesized as free peptides and tested for their ability to inhibit specific IgE binding to allergen extract discs.Results
None of the pin‐coupled Der p I or Der f I peptides was found by the continuous epitope mapping procedure to bind significantly to specific IgE in the sera of hypersensitive patients. The previously reported Der p I peptide epitopes did not inhibit specific IgE binding to mite extract discs.Conclusion
The specific IgE binding epitopes of the house dust mite allergens Der p I and Der f I are discontinuous in nature.
Fel d I levels in cat anal glands
Authors: DE ANDRADE A. DORNELAS , BIRNBAUM J. , MAGALON C. , MAGNOL J. P. , LANTEAUME A. , CHARPIN D. , VERVLOET D. 
Published: April 2006

SummaryBackground
Major cat allergen Fel d I is produced consistently by skin and by sebaceous glands before being spread on the fur.Objective
Since cats have tubular anal glands secreting sebum, proteins and lipids, we looked at the possible presence of Eel d I in these secretions and compared the levels found to those already reported in other cat tissues or secretions.Methods
Thirty‐seven cats were studied. Eel d I dosage in the anal sacs’ secretions was performed using an enzyme linked immunosorbent assay (ELISA) method and total protein evaluation by the Bradford's method.Results
The geometric mean Eel d I concentration was 41 U/g secretion which represents 3.4% of the total protein levels. This amount is the highest ever reported in cat tissues or secretions.Conclusion
The close association of Eel d I protein with skin sebaceous glands and anal sacs both with holocrine function and lipids’ secretions in one hand, and the homology of chain I of Eel d I with some steroid‐binding proteins in other hand, suggest a possible physiological role for Eel d I in the regulation of lipids on skin and cat fur.