bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased positivity of skin test and allergenic stability of glycerinated soybean hull extracts
Authors: Morell  , Codina  , Rodrigo  
Published: March 2003

BackgroundResults obtained from previous experiences with soybean hull antigens suggest that the addition of glycerine to the extract increases positivity of the skin test.ObjectiveThe purpose of this study was to investigate the effect of this glycerine addition and the influence of different storage temperatures on the potency of soybean hull extracts.MethodsTwenty‐two asthmatic patients admitted to emergency rooms during one of the soybean‐related Barcelona asthma epidemics were evaluated 2 years after the last epidemic for: (1) sensitivity to prick test with glycerinated and non‐glycerinated extracts, both fresh and stored at 4 °C, − 20 °C and − 70 °C for 30 days, and (2) specific IgE to a fresh hull extract. All extracts were also studied by sodium dodecyl suphate‐polyacrylamide gel electrophoresis (SDS‐PAGE).ResultsNo differences in positivities were detected for prick tests performed the same day of preparation between non‐glycerinated (5/22; 22.7%) and glycerinated (4/22; 18.2%) extracts. After 30 days storage, positivities of prick test with non‐glycerinated extracts stored at 4 °C did not significantly differ from the results obtained on the first day. However, prick tests performed with glycerinated extracts stored for 30 days showed increased positivity for the extracts stored at 4 °C (7/22; 31%) (P < 0.05) as well as for those stored at − 20 °C and − 70 °C (9/22; 40.9%) (P < 0.001). This latter percentage is similar to that of specific immunoglobulin E detected by radioimmunoassay (10/22; 45.4%). Also, for the glycerinated extracts only, the quantitative response showed an increase in mean diameter of the induration at 30 days at the three temperatures, even though owing to the great standard deviation and limited number of patients, it was only significant for the extract stored at − 20 °C (P < 0.01). SDS‐PAGE gel densitometry at 30 days demonstrated a loss of protein in the bands with a molecular weight higher than 66.2 kDa for non‐glycerinated extracts stored at 4 °C.ConclusionsThe results of this study confirm previous observations with soybean hull allergen extracts and indicate that (1) storage of soybean hull extracts with glycerine addition for 30 days at the concentration studied (1:100 w/v) determines a significant increase in the positivity of skin tests, and (2) glycerine addition stabilizes soybean hull extracts at any of the temperatures studied.
Identification of a highly promiscuous and an HLA allele‐specific T‐cell epitope in the birch major allergen Bet v 1: HLA restriction, epitope mapping and TCR sequence comparisons
Authors: FRIEDL‐HAJEK  , SPANGFORT  , SCHOU  , BREITENEDER  , YSSEL  , JOOST VAN NEERVEN  
Published: March 2003

BackgroundAllergen‐specific CD4+ T cells play an important regulatory role in atopic allergy.ObjectiveTo investigate the human leucocyte antigen (HLA) restriction and T‐cell receptor (TCR) usage of allergen‐specific T‐cell clones (TCCs) that react with defined epitopes of Bet v 1, the major birch pollen allergen.MethodsFive Bet v 1‐specific TCCs derived from two birch pollen‐allergic individuals and specific for Bet v 1, were epitope‐mapped with overlapping synthetic peptides. In addition, HLA‐restriction and TCR CDR3 sequences were determined.ResultsThree TCCs reacted with a Bet v 1 peptide containing amino acid residues 21–33 (BP21), the other two TCCs reacted with a minimal peptide comprising residues 37–45 (BP37). Studies using neutralizing anti‐HLA‐monoclonal antibodies and HLA‐typed APCs showed that the BP37‐specific TCCs were resticted by a HLA‐DQA1*0301/DQB1*0603 heterodimer. In contrast, BP21 was recognized in a highly promiscuous manner. TCCs recognizing this sequence were restricted by HLA‐DPB1*0201, a HLA‐DQA1*0201/DQB1*0201 heterodimer, or HLA‐DRB3*0101. Reverse transcription‐polymerase chain reaction with primers for all known TCRAV and TCRBV gene segments, followed by CDR3 region sequencing, revealed the usage of five different TCRAV and four different TCRBV gene segments by the TCCs, as well as diversity in the joining region. All BP21‐specific TCCs contained a negatively charged residue in their CDR3α regions, the CDR3β regions showed a high concentration of polar and OH‐group bearing residues. BP37‐specific TCCs shared the amino acid combination LY in the middle of their CDR3α regions, the CDR3β regions showed high concentration of OH‐group bearing or charged residues.ConclusionsThis study shows the existence of a highly promiscuous T‐cell epitope in Bet v 1. The presence of additional T‐cell epitopes in Bet v 1 may, however, hamper the clinical applicability of the epitope. Likewise, the diversity in TCR usage by T cells recognizing the epitope does not support the development of TCR‐directed immunotherapy for birch pollen allergy.
Urticaria from beer: an immediate hypersensitivity reaction due to a 10‐kDa protein derived from barley
Authors: Curioni  , Santucci  , Cristaudo  , Canistraci  , Pietravalle  , Simonato  , Giannattasio  
Published: March 2003

BackgroundUrticaria from beer has been reported in atopic patients. In these subjects, the skin‐prick test positivity to and presence of specific serum immunoglobulin (Ig)E for barley malt, the basic ingredient used in brewing, suggested a type I hypersensitivity to barley component(s).ObjectiveTo identify the beer allergen(s) and to investigate the presence of related proteins in barley.MethodsThree patients with urticaria from beer and other atopic people, some of them suffering from baker's asthma, were examined for both prick test sensitivity to and the occurrence of serum‐specific IgE for partially purified proteins from beer. Allergen identification in beer, malt and barley was performed by immunoblotting.ResultsSkin‐prick tests and detection of specific IgE by both solid‐phase (RAST) and liquid‐phase (AlaSTAT) assays demonstrated that the 5–20‐kDa beer protein fraction contained the allergen. Immunoblot analysis with sera of patients with urticaria from beer showed that IgE bound only the 10‐kDa protein band in beer and malt, whereas a main 16‐kDa protein was revealed in barley in addition to a very faint 10‐kDa band. With the serum of a patient suffering from baker's asthma no IgE binding bands were observed in beer, whereas specific IgE binding to several proteins, including a major 16‐kDa component, were detected for both malt and barley.ConclusionsUrticaria from beer is an IgE‐mediated hypersensitivity reaction induced by a protein component of approximately 10 kDa deriving from barley. This allergen does not seem to be related to the major barley 16‐kDa allergen responsible for baker's asthma. Because of the severity of the allergic manifestations to beer we recommend testing atopic patients positive to malt/barley and/or who exhibit urticarial reactions after drinking beer for their sensitivity to this beverage.
Sputum cellular and cytokine responses to inhaled endothelin‐1 in asthma
Authors: Chalmers  , Macleod  , Thomson  , Little  , Patel  , Mcsharry  , Thomson  
Published: March 2003

BackgroundEndothelin (ET)‐1 is a 21‐amino acid peptide which has potent bronchoconstrictor activity. Animal studies show elevation of ET‐1 during experimental airway inflammation, and inhibition of inflammation by endothelin‐antagonists, suggesting pro‐inflammatory activity for ET‐1.ObjectiveWe wanted to assess any acute influence that bronchoconstrictor doses of inhaled ET‐1 might have on cells, tumour necrosis factor (TNF)‐α, interleukin (IL)‐1β, nitrite (NO2) and albumin in induced sputum in asthma.MethodsBronchial challenge was performed using nebulized ET‐1 (nebulized dose range 0.96–15.36 nmol) and placebo in 10 adult asthmatic subjects in a randomized double‐blind placebo‐controlled cross‐over study. Sputum induction was performed 30 min and 4 h after placebo or ET‐1 bronchial challenge.ResultsAll subjects experienced dose‐dependent bronchoconstriction to inhaled ET‐1 with a mean (range) PC15 forced expiratory volume in 1 s (FEV1) to ET‐1 of 9.45 (1.2–21.7) nmol. Comparing ET‐1 with placebo inhalation, there was no change in sputum differential cell counts, TNFα, IL‐1β, NO2 or albumin at 30 min or 4 h after inhalation, nor was there a difference in these parameters at 4 h compared with 30 min after ET‐1 inhalation. There was no fall in FEV1 at 4 h after ET‐1 inhalation, suggesting that ET‐1 inhalation is not associated with a late bronchoconstrictor response.ConclusionsWe conclude that inhaled ET‐1 does not appear to stimulate an acute inflammatory response in asthma as assessed by differential cell count, TNFα, IL‐1β, NO2 and albumin concentrations in induced sputum.
Endothelial cells upregulate eosinophil superoxide generation via VCAM‐1 expression
Authors: NAGATA  , SEDGWICK  , VRTIS  , BUSSE  
Published: March 2003

Background In vitro eosinophil (EOS) adhesion to recombinant human (rh)‐vascular cell adhesion molecule (VCAM)‐1 stimulates superoxide anion (O2−) generation and enhances formyl‐methionyl‐leucyl phenylalanine (FMLP)‐activated O2− generation. Therefore, EOS adhesion via VLA‐4 to VCAM‐1 expressed on endothelium may be instrumental in the selective recruitment and function of EOS in airway inflammation.ObjectiveWe hypothesized that EOS interaction with endothelial cells expressing VCAM‐1 will undergo an enhancement in inflammatory function.MethodsTo determine this possibility, human umbilical vein endothelial cells (HUVEC) were stimulated with either a combination of interleukin (IL)‐4 and tumour necrosis factor (TNF)‐α (100 p M) or medium alone for 24 h; the expression of adhesion proteins on HUVEC and their effect on EOS O2− generation was subsequently determined.ResultsAs determined by both enzyme‐linked immunosorbent assay and flow cytometry, IL‐4 and TNFα acted synergistically to induce VCAM‐1 expression on HUVEC. Treating HUVEC with IL‐4/TNFα also increased EOS adhesion and primed subsequent FMLP (0.1 μM) activated EOS O2− generation. Although EOS adhesion was partially inhibited by both antiα4 and antiβ2 monoclonal antibodies (MoAbs), O2− generation was completely inhibited by either antiα4 integrin MoAb (HP1/2) or anti‐VCAM MoAb (BBIG‐V1). Furthermore, enhanced O2− generation, but not adhesion, associated with IL‐4 + TNFα‐treatment of HUVEC was inhibited when EOS were treated with the platelet activating factor (PAF)‐antagonist WEB 2086 (20 μM), thus suggesting an involvement of PAF in priming EOS. However, paraformaldehyde fixation of IL‐4/TFN‐α treated HUVEC did not significantly alter EOS function.ConclusionsThese results suggest EOS adhesion to endothelial cells via an VLA‐4/VCAM–1 interaction may be important in the development of the function of this cell. Furthermore, our results suggest that modulation of EOS function involves two priming factors: EOS adhesion to HUVEC expressing VCAM‐1 and PAF.
Functional interleukin‐5 activity in peripheral blood mononuclear cells from adolescents with mite antigen asthma in remission
Authors: NOMA  , HAYASHI  , KAWANO  , YOSHIZAWA  , ISHIKAWA  , SAEKI  , AOKI  , MATSUURA  
Published: March 2003

BackgroundAsthma improves in most children during adolescence such that a small minority of patients exhibit clinically significant symptoms by the age of 20 years.Objective and methodsTo investigate late allergic reactions, including eosinophil inflammation, associated with outgrowing mite antigen‐induced bronchial asthma during adolescence, the relationship between clinical status and functional activity of interleukin (IL)‐5 produced by Dermatophagoides farinae (Df)‐stimulated peripheral mononuclear cells (PBMCs) in culture was assessed in mouse IL‐3‐dependent cells transfected with the human IL‐5 receptor gene.ResultsActivity of IL‐5 spontaneously produced by PBMCs from either patients with mite‐sensitive bronchial asthma or nonatopic control subjects was low. The activity of IL‐5 produced by PBMCs stimulated with concanavalin A was significantly higher. Upon challenge with specific allergens, such as Df antigen, but not with irrelevant antigens, including ovalbumin, the in vitro activity was increased in patients with active disease and decreased in patients in remission.ConclusionResults suggest that the antigen‐specific up‐regulation of functional IL‐5 activity in late allergic reactions is reduced in patients in remission and likely to result in an improvement in clinical status. The Df antigen may suppress Df‐induced responses in patients with asthma in remission.
Elevated cord serum IgE increases the risk of aeroallergen sensitization without increasing respiratory allergic symptoms in early childhood
Authors: Tariq  , Arshad  , Matthews  , Hakim  
Published: March 2003

BackgroundIncreasing prevalence of allergic disorders has focused attention on primary prevention. There is a need to improve the accuracy of early‐life predictors of atopy so that the at‐risk population can be accurately defined and preventive measures instituted.ObjectiveThe predictive capacity of elevated cord IgE, with or without family history of atopy, to allergic symptoms and skin prick test (SPT) sensitization is evaluated in a birth cohort followed up prospectively for 4 years.MethodsA birth cohort of 1456 consecutively born children was recruited in 1989. Data were collected on family history of atopy and cord serum total IgE (cord IgE) was measured. Of these, 1218 children were seen in the clinic at 4 years to determine the development of symptoms and signs of allergic disease and 981 were skin tested to a range of common food and aeroallergens.ResultsOf 1218 children reviewed at age 4 years, 218 (17.8%) had symptoms of respiratory allergy and, of those skin tested (n = 981), 192 (19.6%) reacted positively. Twice as many children with elevated cord IgE (≥ 0.5 kU/L) at birth became sensitized to aeroallergens by age 4 years (34.8% vs 17.3%, P < 0.001). Positive predictive value (PPV) of elevated cord IgE for the development of aeroallergen sensitization was better than that of family history of atopy (34.8 vs 22.6%). Combining paternal atopy with elevated cord IgE substantially increased the predictive capacity (PPV 77.8%). Cord IgE levels did not correlate with clinical asthma or rhinitis at age 4 years and PPV for allergic respiratory symptoms remained poor at all cutoffs.ConclusionCord IgE is better than family history for predicting atopy as defined by allergen sensitization and this predictive value can be further increased by combining cord IgE with paternal atopy.
Allergy to goat and sheep cheese with good tolerance to cow cheese
Authors: Umpiérrez  , Quirce  , Marañón  , Cuesta  , García‐Villamuza  , Lahoz  , Sastre  
Published: March 2003

BackgroundWe report on a patient who experienced allergic reactions after eating goat cheese and after touching goat and sheep cheese, but not after consuming cow's milk dairy products.ObjectiveTo assess the allergenicity and IgE‐binding capacity of the caseins from the three different species.MethodsSkin prick tests were carried out using whole milk and caseins from three different species (goat, sheep and cow), and whey fractions of cow's milk. Total serum IgE and specific IgE to cow's milk proteins were measured by CAP system and specific IgE against caseins and whole milk were determined by ELISA technique. To evaluate allergenic cross‐reactivity, inhibition of the IgE ELISA activity to goat's milk and goat casein was tested for the three caseins. SDS‐PAGE and immunoblotting was used to determine IgE binding bands in caseins.ResultsSkin tests were positive to sheep and goat's milk, sheep and goat casein, as well as to sheep and goat cheese. Total serum IgE was 66 kU/L and IgE determinations by CAP were negative. IgE ELISA against the caseins from goat and sheep was strongly positive, whereas it was negative to cow casein. ELISA inhibition assays revealed a high degree of cross‐reactivity between goat casein and sheep casein. Immunoblotting showed three IgE‐binding bands in goat casein at 31, 27 and 22 kDa, which may correspond to α‐, β‐ and γ‐caseins. A band at about 31 kDa was observed in sheep casein and another band at 34 kDa was recognized in cow casein.ConclusionThis patient developed allergy to goat and sheep cheese with good tolerance to cow's milk. We identified goat casein as the main allergen causing sensitization in this patient as demonstrated by in vivo and in vitro tests. A high degree of cross‐reactivity between goat and sheep casein was observed.
Increased mast cell tryptase in sudden infant death — anaphylaxis, hypoxia or artefact?
Authors: Edston E. , Gidlund E. , Wickman M. , Ribbing H. , Van Hage‐Hamsten M. 
Published: March 2003

BackgroundIncreased concentrations of mast cell tryptase in post mortem blood have frequently been observed in sudden infant deaths but the cause of this has not yet been clarified.ObjectiveThe aim was to evaluate factors (immunological, morphological and anamnestic data) behind the observed increase in mast cell tryptase in sudden infant deaths with elevated tryptase.MethodsMast cell tryptase and total immunoglobulin (Ig) E were measured in post mortem sera from 44 infants younger than 1.5 years. Radioallergosorbent tests were performed for possible allergens (mixture for relevant food allergens, Phadiatop and latex). IgG subclasses, IgM, and complement factors (C3, C4 and factor B) were measured with radial immunodiffusion. Mast cells, labelled with antibodies against mast cell tryptase, were counted in the lungs and heart. The circumstances of death and medical history of the deceased infant and family were obtained through police and hospital records.ResultsIn 40% of the SIDS cases tryptase was elevated (>10 μg/L). Total IgE in serum was increased in 33% compared with clinical reference values but showed no association with mast cell tryptase. RAST tests were positive in three cases. In one of these cases both tryptase and total IgE were elevated. The only variable that was associated with high tryptase values was prone position at death (P ≤ 0.05 ). Allergy or asthma in the family were alleged in 50% of the cases, but was not associated with elevated tryptase or IgE. Children with elevated total IgE also displayed high concentrations of IgG1 and IgG2. Infants who died in the spring had significantly higher IgE than the others (P ≤ 0.05).ConclusionThe results do not support the hypothesis that the elevated tryptase concentrations in sudden infant death are caused by allergy. The association between prone position at death and elevated tryptase could hypothetically be explained by mast cell degranulation due to, for example, a hypoxic stimulus in these infants.
Airway inflammation and altered alveolar macrophage phenotype pattern after repeated low‐dose allergen exposure of atopic asthmatic subjects
Authors: Lensmar C. , Prieto J. , Dahlén B. , Eklund A. , Grunewald J. , Roquet A. 
Published: March 2003

BackgroundThe alveolar macrophage (AM) constitutes an important link between pulmonary innate and adaptive immunity due to its antigen‐presenting capacity and ability to express different immunomodulating mediators. The role of AMs in the pathogenesis of allergic inflammation has yet to be fully determined.ObjectiveTo investigate clinical effects and any change in the AM phenotype pattern after inhalation of sub‐clinical doses of allergen by asthmatic patients.MethodsEight subjects with allergic asthma underwent repeated low‐dose allergen provocations equivalent to 10% of PD20. AMs recovered with bronchoalveolar lavage (BAL) were characterized by flow cytometric analysis of adhesion molecules, co‐stimulatory molecules and markers for AM population activation and heterogeneity.ResultsAn allergic airway inflammation, sub‐clinical in six out of eight subjects, was obtained after low‐dose allergen provocations, as determined by increased airway methacholine reactivity, increased BAL fluid total cell and eosinophil counts and increased serum ECP levels. The AMs showed a post‐challenge altered phenotype pattern with a decreased expression of CD11a, CD16, CD71 and HLA class I and an increased expression of CD11b and CD14. The AMs were positive for CD83 and a weak post‐challenge increase in the CD83 expression was found.ConclusionRepeated low‐dose allergen exposure induces an allergic airway inflammation in asthmatic subjects. The inflammation is associated with an altered AM phenotype pattern, consistent with an influx of monocytes and a hypothetical increased accessory cell function in the airways, possibly contributing to the development and sustenance of airway inflammation in asthma.
Influence of bronchial allergen challenge on histamine release by human basophils
Authors: Lie  , Van Der Veen  , Knol  , Mul  , Jansen  , Roos  , Van Der Zee  
Published: March 2003

BackgroundBasophils can be primed by cytokines such as interleukin (IL) ‐3, IL‐5 or granulocyte macrophage‐colony stimulating factor (GM‐CSF). It has been described that the concentrations of these cytokines are enhanced at sites of allergic inflammation as well as systemic in allergic asthma.ObjectiveTo investigate the priming status of basophils as detected by thapsigargin‐induced histamine release during bronchial allergen challenge.MethodsTen subjects allergic to house dust mite were challenged via an aerosol delivery system. Spontaneous leucocyte histamine release as well as histamine release induced by various stimuli was measured in vitro at several time points. In addition, lung function parameters, serum IL‐5 and blood eosinophil counts were evaluated.ResultsWe found no effect of bronchial allergen challenge upon spontaneous leucocyte histamine release, nor upon histamine release induced by anti‐immunoglobulin (Ig) E, house dust mite extract, C5a, fMLP, IL‐3, PMA+ thapsigargin or IL‐3+ thapsigargin. However, the priming status of basophils as measured by thapsigargin‐induced histamine release was enhanced at 24 h after bronchial allergen challenge. Analysis of the individual data showed a heterogeneous initial response (30 min, 6 h) followed by a predominant increase at 24 h after allergen challenge. This increase in the thapsigargin‐induced histamine release correlated with the increase in serum IL‐5 levels at 24 h after allergen challenge.ConclusionThe priming status of human basophils as measured by thapsigargin‐induced histamine release is enhanced 24 h after allergen challenge.
Eosinophilic tracheobronchitis and airway cough hypersensitivity in chronic non‐productive cough
Authors: Fujimura  , Ogawa  , Yasui  , Matsuda  
Published: March 2003

BackgroundWe have shown that some patients presenting with chronic bronchodilator‐resistant non‐productive cough have global atopic tendency and airway cough hypersensitivity without non‐specific bronchial hyperresponsiveness, abbreviated as atopic cough. The cough is successfully treated with histamine H1‐antagonists and/or glucocorticoids.ObjectiveThis prospective study was conducted to elucidate the histological feature of atopic cough.MethodsTracheal and bronchial mucosa obtained by transbronchoscopic biopsy and bronchoalveolar lavage (BAL) cell component were studied with special emphasis on eosinophils in eight non‐smokers diagnosed with atopic cough, all of whom had increased sensitivity of cough response to inhaled capsaicin, normal lung function and bronchial responsiveness to methacholine and normal chest roentgenogram. Their cough completely resolved on histamine H1‐antagonists and/or glucocorticoids. Transbronchoscopic tracheal and bronchial biopsy and BAL were also performed in healthy non‐smokers as a control.ResultsA small number of eosinophils was detected in subepithelium of trachea in six of seven patients and in subepithelium of bronchi in seven of eight cough patients. The numbers of eosinophils in subepithelium of trachea and bronchi were significantly increased in the patients compared with control subjects. There was no BAL eosinophilia in any patients.ConclusionIt is concluded that eosinophilic tracheobronchitis and cough hypersensitivity are pathological and physiological characteristics of atopic cough.