bluuebunny/crossref_metadata_2025_split huggingface dataset:
Identification of monocyte chemotactic factors in supernatants of ovalbumin‐stimulated lymphocytes from patients with atopic dermatitis who are sensitive to hen's egg
Authors: FUKUTOMI O. , KONDO N. , AGATA H. , SHINODA S. , KUWABARA N. , SHINBARA M. , INOUE R. , ORII T. 
Published: April 2006

SummaryMonocyte chemotactic activities in supernatants of ovalbumin (OA)‐stimulated peripheral blood mononuclear cell (PBMC) cultures were studied in patients with atopic dermatitis (AD) who were sensitive to hen's egg. The monocyte chemotactic activities in hen's egg‐sensitive AD patients were significantly higher than those of non‐atopic healthy controls and patients with immediate allergic symptoms. However, the monocyte chemotactic activities were not detected in bovine serum albumin‐Stimulated PBMC culture supernatants in patients with AD who were sensitive to hen's egg. but not to cow's milk. Furthermore, there was significant correlation between the monocyte chemotactic activities and proliferative responses of PBMCs to OA in hen's egg‐sensitive AD patients, whereas there was no significant correlation between the monocyte chemotactic activities and radioallergosorbent test values. These results suggest that PBMCs stimulated with food antigens produce monocyte chemotactic factors which relate to the pathogenesis of AD in food‐sensitive AD patients and that the pathogdenesis of AD may be related to cell‐mediated immune responses.
Safety and efficacy of a 12‐week maintenance interval in patients treated with Hymenoptera venom immunotherapy
Authors: KOCHUYT A.‐M. , STEVENS E. A. M. 
Published: April 2006

SummaryIt is currently recommended to administer a maintenance dose of 100 μg of venom at 4–6 week intervals for Hymenoptera venom immunotherapy (VIT), Because the optimal duration of therapy is not known, we decided to progressively prolong the interval between maintenance injections instead of accepting the risk of anaphylactic reactions when VIT is discontinued after a predetermined period. We report here on the results of a first phase of this interval extension programme, covering the gradual increase of the interval from 1‐12 weeks over 19 months in 178 patients. A 12‐week interval maintenance VIT could be achieved in 117/128 (91%) of yellow jacket venom (YJV) and in 35/50(70%) of honeybee venom (HBV) allergic patients. At the lime of the interview these 152 patients had been treated with 12‐weekly 100 μg venom injections for an average period of 2 years without any untoward reaction to VIT. During this period of 48 YJV allergy sufferers experienced 77 field re‐stings without systemic reaction (SR), and 17 HBV allergic subjects were restung at least 213 times in total, with one patient developing a very large local reaction and one a mild systemic reaction. In 26 of the 17S patients the interval of 12 weeks was not reached for various reasons, with a higher failure rate among the HBV allergic patients. Most Hymenoptera venom allergic patients can thus be safely and effectively treated with 12‐weekly injections of 100 μg venom.
High anti‐IgE levels at birth are associated with a reduced allergy prevalence in infants at risk: a prospective study
Authors: VASSELLA C. C. , ODELRAM H. , KJELLMAN N.‐I. M. , BORRES M. P. , VANTO T. , BJÖRKSTEN B. 
Published: April 2006

SummaryDevelopment of atopic disease was prospectively studied in 148 children from birth to the age of 18 months and related to serum levels of IgG anti‐IgE antibody. Children with a dual heredity of allergy, but remaining healthy, had significantly higher IgG anti‐IgE levels at birth than children with a similar predisposition to allergy, who became allergic. Children with increased allergy risk, defined by elevated IgE levels at birth (>= 0.53 kU/l) and with probable allergy symptoms had also significantly higher IgG anti‐IgE levels at birth than children of the same risk group, developing definite allergy. Independent of allergy risk, there was a significantly lower prevalence of atopic disease in children with cord serum levels of IgG anti‐IgE above 350AU.1 than in children with lower levels. Additionally, we showed that the allergy predictive capacity of IgE levels in cord serum was slightly improved in specificity, sensitivity and efficiency by including not only the family history of allergy, but also cord serum levels of IgG anti‐IgE. Our results thus raise the possibility that high levels of IgG anti‐IgE protect children of increased allergy risk from early development of atopic disease and reduce the severity of symptoms.
Immediate hypersensitivity to bakery, brewery and wine products in yeast‐sensitive atopic dermatitis patients
Authors: KORTEKANGAS‐SAVOLAINEN O. , SAVOLAINEN J. , LANTTO R. , KALIMO K. 
Published: April 2006

SummaryUltrafiltered (> 1000 Da) samples of beer, aged red wine, young white wine, sparkling wine and extracts of fresh wheat bread and dried rye bread were analysed by skin‐prick test (SPT), radioallergosorbent test (RAST) inhibition, sodium dodecylsulphate‐polyacrylamide gel electrophoresis (SDS‐PAGE) and immunoblotting to find out if they contain Saccharomyces cerevisiae(S. cerevisiae, baker's yeast) allergens. Serum pool consisting of S. cerevisiae positive sera was used in the assays. The results were compared with freeze‐dried reference. V. cerevisiae and cereal antigens. The beer, bread, red wine and sparkling wine extracts elicited immediate reactions. However, no evident correlation with suspected symptoms was observed. White wine extract caused reactions in four out of six atopic dermatitis (AD) patients with symptoms, and in five out of seven symptom‐free AD patients and in two of the 24 controls. In SDS‐PAGE, protein bands were found in wheat and rye bread extracts and beer. In IgE immunoblotting, however, no staining was seen with the S. cerevisiae positive sera suggesting that they were of cereal origin. In white wine and champagne extracts a nonspecific staining was seen in the region 20kDa representing, e.g. lectin‐like activity. No bakers yeast antigen could be detected in brewery and bakery products with IgE‐immunoblotting even in the excessively concentrated extracts. The IgE mediated allergy to baker's yeast alone should thus not lead to denial of bakery, brewery and wine products.
Effect of grain exposure and smoking on the longitudinal changes in immediate skin reactivity
Authors: LIN F. J. , KENNEDY S. M. , CHAN‐YEUNG M. 
Published: April 2006

SummaryThe study was carried out to investigate the effect of occupational exposure and smoking on the longitudinal changes of immediate skin reactivity over 3 years in working populations. A total of 480 grain elevator workers and 707 transit and ferry (control) workers were included because they had allergy skin tests on both surveys. Skin‐prick texts using three common allergens and a negative and histamine controls were administered during both surveys. The reaction was considered positive if the mean weal size was 3 mm or greater than that of the negative control. Conversion was defined as a change from the non‐atopic state in the initial survey to the atopic state in the follow‐up survey. Reversion was defined as a change from the atopic state in the initial survey to the non‐atopic state in the follow‐up survey. The findings showed that grain workers had two times risk of conversion than control workers. Recent smokers, who changed their habit from non‐smoker/ex‐smoker to smoker in the follow‐up survey, were at a three times risk of conversion than non‐smokers. The reversion of skin‐test reactivity was not associated with age, smoking habits, or working exposure. When investigating studies of longitudinal changes in immediate skin reactivity, the effects of age, changes in smoking habit and occupational exposure should be considered.
House dust mite allergen avoidance: a randomized controlled trial of surface chemical treatment and encasement of bedding
Authors: MARKS G. B. , TOVEY E. R. , GREEN W. , SHEARER M. , SALOME C. M. , WOOLCOCK A. J. 
Published: April 2006

SummaryTo test the effectiveness of a house dust mite (HDM) allergen avoidance strategy we conducted a randomized controlled trial in 35 atopic subjects with asthma, aged 13 to 60 living in Sydney — a high HDM allergen environment. After a 3 month run‐in period, subjects were randomized to active allergen avoidance treatment (n= 17) or placebo (n= 18) groups and followed for 6 months. The active treatment involved placing impermeable covers over the mattress, pillows and duvet and spraying the remaining bedding, as well as the carpets and furniture, with a tannic acid/acaricidal spray. Subjects kept a daily record of symptoms and peak expiratory flow rates and had 3 monthly assessments of lung function and airway hyperresponsiveness (AHR). Dust samples were collected from the bed, the bedroom floor and the living room floor at 3 monthly intervals and 2 weeks after the treatment. Mean HDM allergen levels at baseline at these sites were, in the active group, 15.5, 9.6 and 10.2μ/g Der p I/g of fine dust, and, in the placebo group 25.7, 11.8 and 6.3μg/g. Two weeks after the allergen avoidance treatment the HDM allergen level in the beds was reduced to 29% of baseline (95% CI 16.50%, P= 0.038 compared with placebo), but was not significantly different at 3 or 6 months. There was also no significant effect of the allergen avoidance treatment on symptom scores, peak flow variability, lung function or AHR (P > 0.1). We conclude that, in a high HDM allergen environment, simple chemical treatment and encasement of bedding is not sufficient to cause a sustained, beneficial reduction in allergen levels. Effective allergen avoidance requires an active strategy to remove allergen reservoirs and control accumulating allergen within the house.
An increased frequency of IgE‐producing B cell precursors contributes to the elevated levels of plasma IgE in atopic subjects
Authors: KASAIAN M. T. , MEYER C. H. , NAULT A. K. , BOND J. F. 
Published: April 2006

SummaryBackground: The production of specific IgE, which underlies the allergic response, may be a normal correlate of the immune response to a certain class of antigen (allergens), or could represent a unique response driven by regulatory signals that are absent in non‐allergic individuals. If atopic subjects do possess a regulatory environment favoring IgE production, they may display not only allergen‐specific IgE, but also higher levels of total IgE and higher frequencies of IgE‐producing B lymphocytes.Objective: To address the contribution of antibody‐producing cell number to the circulating IgE titre in atopic vs non‐atopic subjects.Methods: Frequency determination by limiting dilution of EBV transformants and Poisson distribution analysis. Titres of total and allergen‐specific IgM, IgG, and IgE by specific ELISA.Results: In contrast to findings reported by others, the atopic subjects had a significantly higher frequency of IgE‐producing B cells than non‐atopies (0.79% of total Ig‐producing cells, as compared with 0.17% for the control group; P < 0.01), suggesting that one factor contributing to the high plasma IgE titres in atopic subjects is the high frequency of B lymphocytes with the potential to produce IgE. Although only the atopic subjects produced allergen‐specific IgE, the frequency of specific IgE‐producing B cells was undetectable in both groups.Conclusion: Atopic subjects have higher frequencies of IgE‐producing B cell precursors than non‐atopies. A correlation exists between IgE‐producing B cell frequency and levels of circulating IgE.
Bee venom immunotherapy induces a shift in cytokine responses from a TH‐2 to a TH‐1 dominant pattern: comparison of rush and conventional immunotherapy
Authors: McHUGH S. M. , DEIGHTON J. , STEWART A. G. , LACHMANN P. J. , EWAN P. W. 
Published: April 2006

SummaryBackground: The mechanism of immunotherapy is unclear. Allergic disease is known to involve enhanced TH‐2 cytokine responses to allergen.Objective: In order to investigate the mechanisms of immunotherapy, we have examined changes in cytokine secretion before (13 patients) and during (nine patients) both rush and conventional venom immunotherapy (VIT) in nee venom allergic patient. Method Peripheral blood mononuclear cells were stimulated in vitro with see venom, non‐specific antigen or mitogen and secretion of IL‐4 (TH‐2) and IFNγ (TH‐1) over the culture period measured.Results: Untreated patients had TH‐2 responses to venom and TH‐1 responses to antigen and strong proliferative responses to venom. Controls showed no response (proliferation or cytokines) to venom and the normal TH‐1 response to antigen. VIT resulted in marked changes in cytokine secretion to venom, with reduction of the abnormal TH‐2 response and induction of a TH‐1 response. The pattern differed in rush and conventional VIT. One day after rush VIT there was a significant fall in IL‐4 secretion (P < 0.01), which rose by 3 weeks then declined. In conventional ViT there was a gradual reduction of IL‐4 production significant after 2 months and undetectable by 6 months. IFNγ secretion was induced by VIT. Proliferative responses mirrored the IL‐4 changes. One day after rush VIT there was a loss of T cells, monocytes and NK cells from peripheral blood.Conclusion: This study shows that immmotherapy shifted cytokine responses to allergen from a TH‐2 to a TH‐1 dominant pattern, suggesting direct effects on T cells. How these cytokine changes relate to clinical desensitization is not clear. In the longer term they would result in an isotype switch from IgE to IgG. Early changes in cytokine or chemokine production might down regulate mast cell or basophil reactivity and explain the rapid desensilization in rush VIT.
Challenge of mast cells with increasing amounts of antigen induces desensitization
Authors: SHALIT M. , LEVI‐SCHAFFER F. 
Published: April 2006

SummaryBackground
In vivo rush desensitization is a procedure widely employed to quickly desensitizo allergic patients by administering increasing doses of the offending antigen at short intervals. The mechanism(s) underlying this process and the possible role of mast cells in it have not been well delineated.Objective
To define an ex vivo model for rush desensitization utilizing the mast cell‐fibroblast coculture system.Methods
Rat peritoneal mast cells were cultured on 3T3 fibroblasls and were pre‐incubated with saturating or suboptimal concentrations of IgE anti‐DNP antibodies. Mast cells were then repeatedly challenged at 30 min intervals, with increasing amounts (0.001 100ng/mL) of the antigen DNP‐HSA, in the presence of calcium ions. Parallel control cultures were stimulated only once by each antigen concentration. In another set of experiments, mast cells were repeatedly activated with increasing concentrations (0.1‐1000 ng/mL) of compound 48/80. Supernatants and cell sonicates were assessed for histamine content and the percentage of histamine released was calculated.Results
When saturating concentrations of IgE anti‐DNP antibodies were used, mast cells challenged repeatedly with DNP‐HSA did not release significant amounts of histamine up to an antigen concentration of I ng/mL. At this stage they were partially desensitized, releasing only 108.3 . 17.1 ng histamine/plate (7.9±0.8%). A marked desensitization was observed at optimal antigen concentration (100 ng/mL). where experimental mast cells released only 45.6±10.9ng/plate, compared with 661.9±48.2ng/plate in firstly challenged cultures. Desensitization was probably not due to mast cells histamine depletion, since the cells still contained large amounts of histamine (579.5±108.6ng/plate) at the end of the procedure. A similar pattern of desensitization was observed when mast cell were preincubated with a subotimal concentration of IgE antibodies. Activation of mast cells with increasing amounts of the IgE‐independent secretagogue, compound 48/80. did not cause desensitization since at each concentration both repetitively challenged and control cultures released similar amounts of histamine. Furthermore, challenge of antigen‐desensitized mast cells with compound 48/80 caused the release of 75.9±4.9% histamine comparable to the percentage of histamine released from controls (79.5±6.7).Conclusion
Repeated exposure of mast cells to gradually increasing amounts of antigen induces their refractoriness. This observation would suggest a role for mast cells in rush desensitization procedure in vivo. Our coculture system may serve as a useful model for studying this process.
Epidemiology of the effects of air pollutants on allergic disease in children
Authors: Carswell F. 
Published: April 2006

Summary 9.21. Extensive studies now indicate that many atmospheric pollutants can provoke respiratory symptoms. Usually a complex mixture affects children but it seems that ozone, particulates and nitrogen dioxide are virtually certainly implicated and the organic substances released with dense traffic are likely to be involved. There is commonly difficulty specifically identifying the pollutant because of the complex mixture and their interactive effects. Other environmental conditions such as weather can interact both by increasing the concentration of the pollutant and by increasing the effectiveness of the same concentration of the pollutant and by increasing the effectiveness of the same concentration of pollutants such as particulates. It is only with regard to NO2 where a convenient and easy system of monitoring is available that detailed personal monitoring results are obtainable, so that despite the rather modest effect of NO2 it is well documented, whereas those pollutants which still have to be centrally monitored may have a greater biological effect. All the studies indicate the importance of considering the interactive effects of environmental cigarette smoke as another possible confounder, as is exercise. Although many of the studies imply that atmospheric pollution can produce an increase in clinically apparent infection, it is not established that the symptoms which are analogous to those produce by virus infection are actually produced by a virus infection are actually produced by a virus. Given these difficulties, it is surprising that some evidence with regard to the timing of the effect has been produced; thus suphur dioxide commonly produces a same‐day effect whereas particulates tend to produce a more delayed effect.
Human auto‐anti‐idiotypic antibodies to mite‐specific IgE can degranulate human basophils in vitro
Authors: WEYER A. , LE MAO J. , ETIEVANT M. , DAVID B. , GUINNEPAIN M. T. , SAINT‐REMY J. M. R. 
Published: April 2006

SummaryBackground
Anti‐idiotypic antibodies (anti‐Ids) to specific IgE antibodies are formed spontaneously during an anti‐allergen immune response and can be induced by immunotherapy. Although anti‐Ids can down‐regulate the production of IgF. antibodies, at least in experimental models, their possible role in the modulation of target cell reactivity remains ill‐defined.Objective
The capacity of human anti‐Ids to modulate the release of histamine was examined in an in vitro system of human basophil degranillation. Anti‐Ids were prepared from the serum of six Dermatophagoides pteranyssinus (DP)‐hypersensitive patients suffering from atopic dermatitis and who had never been desensitized. Basophils were obtained from the blood of atopic donors. The extent of histaminc release was determined using a fluorometric assay.Results
We show that: anti‐Ids trigger the release of histamine in an allergen‐specific, dose‐ and IgE‐dependent manner; the release is not due to the presence of allergen and/ or anti‐IgE antibodies: and that the degranulating activity can be removed by absorption with affinity‐purified anti‐Dp antibodies of the corresponding patient.Conclusion
These results indicate that spontaneously produced human anti‐Ids can modulate the reactivity of human basophils.
The lack of effect of benzalkonium chloride on the cilia of the nasal mucosa in patients with perennial allergic rhinitis: a combined functional, light, scanning and transmission electron microscopy study
Authors: BRAAT J. P. M. , AINGE G. , BOWLES J. A. K. , RICHARDS D. H , VAN RIESSEN D. , VISSER W. J. , RIJNTJES E. 
Published: April 2006

SummaryBackground
Controversy still exists about the effect of 0.02% benzalkonium chloride (BKC). a preservative in many nasal sprays, on human nasal epithelium in vivo. Objective To determine the safety of BKC by assessing its effect on the function and morphology of cilia of human nasal epithelium.Methods
A single‐centre, double‐blind nasal biopsy study in 22 patients with perennial allergic rhinitis, receiving fluticasone propionate aqueous nasal spray (FPANS) containing BKC. BKC plus placebo or placebo alone for 6 weeks. Before, at two weekly intervals during treatment and 2 weeks after treatment ceased an indigocarmine saccharine transport time (ICST) was performed. Results ICST results did not significantly vary between the groups. There was no statistical relationship between the number of ciliated cells present and the treatment the patients received. Scanning and transmission electron microscopy examination showed no effects of BKC.Conclusion
Despite reports of its ciliostatic effects in vitro. BKC did not have such an effect when it was applied for 6 weeks (with/without fluticasone propionale) to the nasal mucosa of perennial allergic rhinitis patients in vivo.
Antihistamine activity, central nervous system and cardiovascular profiles of histamine H1 antagonists: comparative studies with loratadine, terfenadine and sedating antihistamines in guinea‐pigs
Authors: HEY J. A. , DEL PRADO M. , CUSS F. M. , EGAN R. W. , SHERWOOD J. , LIN C.‐C. , KREUTNER W. 
Published: April 2006

SummaryBackground
Sedation limits the clinical utility of classical H, antihistamines. while newer antihistamincs such as loratadine and terfenadine arc non‐sedating. However, clinical use of terfenadine has been associated with rare but severe cardiac arrhythmias, in particular lorsades de pointes.Objective
To establish a quantitative experimental model for assessing the sedating and cardiotoxicity potential of non‐sedating and sedating antihistamines.Methods
Drugs were administered intravenously and the integrated amplitude of the conical electroencephalogram (EEC) signal was recorded. The threshold dose that depressed EEG activity was compared with the dose required lo inhibit by 50% the peripheral bronchospasm elicited by 10 μg/ kg i.v., of histamine. In separate studies, the electrocardiogram (ECG) and cardiovascular effects of loratadine (30 and 100mg/kg, i.v.). terfeuadine (10mg/kg. i.v.). promethazine (5mg/kg. i.v.) and diphenhydramine (20 mg kg, i.v.) were evaluated.Results
The sedating antihistamines. diphenhydramine and promethazine. depressed the integrated EEG at doses between 0.6 and 2.0 limes their peripheral antihisiamine doses. Loratadine had no EEG depressant activity at 100 mg kg. i.v., a dose more than I 70 times its LD50 (0.58 mg kg, i.v.) against histamine bronchospasm. We were unable lo evaluate the EEG effects of terfenadine. because it produced cardiovascular collapse at 10 mg/kg. i.v. Loratadine and promethazinc did not produce adverse cardiovascular effects. nor did they alter normal ECG activity. Diphenhydramine produced brady‐cardia followed by a transient hypertensive phase without affecting the QTc interval. In contrast, terfenadine elicited hypotension, bradycardia and significant arrhythmogenic activiy, causing a prolongation of the QTc interval and a torsades de pointes like ventricular arrhythmia. Pharmacokinetic studies after i.v. administration of loraladine (30 and 100 mg/kg) demonstrated plasma levels of loratadine and its major metabolite descarboethoxyloratadine to be several orders of magnitude greater than levels found in humans at the clinical dose of 10mg.Conclusion
The CNS depressant effects of H1 antihislamines arc promcthazine≅ diphenhdramine ≫ loratadine = placebo. Of the non‐sedating antihistamines. loratadine was devoid of adverse cardiovascular effects whereas terfenadine caused a pronounced disruption of the normal ECG. characterized by a torsades de pointes‐like effect.