bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sublingual versus injective immunotherapy in grass pollen allergic patients: a double blind (double dummy) study
Authors: QUIRINO T. , IEMOLI E. , SICILIANI E. , PARMIANI S. , MILAZZO F. 
Published: April 2006

SummaryBackground
Injective immunotherapy is a well‐known and recognized treatment for allergic diseases, but its safety has been questioned during recent years. Alternative administration routes have been proposed and there is a growing interest and experience in sublingual therapy. The safety of alternative routes is nonetheless a real advantage, so long as it is not counterbalanced by a loss of clinical benefit.Objective
We have compared the efficacy of the same biologically standardized grass pollen extract administered through the injective or the sublingual route, in a group of 20 patients followed for two pollen seasons.Methods
Both therapies were administered for 12 months according to a double‐blind (double‐dummy) plan; at the end of the trial the cumulative dosage of the sublingual therapy was 2.4 times higher than that of the injective therapy. Data about skin reactivity, symptoms and drugs scores during the pollen season, as well as total specific IgG and specific IgG4, during and after the trial, were obtained.Results
Our data show that sublingual and injective therapy are equally effective according to subjective clinical parameters, with a statistically highly significant reduction of symptoms and drugs (P= 0.002 for symptoms and drugs in SLIT‐treated patients; P= 0.002 for symptoms and P= 0.0039 for drugs in patients given injections). On the other hand, objective parameters (total specific IgG, specific IgG4, skin reactivity) changed only in patients treated with active injective therapy, with P < 0.001, P < 0.001 and P= 0.021, respectively.Conclusions
The discrepancies observed could be interpreted as a consequence of different mechanisms of action of the two therapies or to the lack of close relationships between the clinical and the objective parameters which were considered here.
Occupational allergy due to spider mites: Tetranychus urticae (Koch) and Panonychus citri (Koch)
Authors: BURCHES E. , PELAEZ A. , MORALES C. , BRASO J.V. , ROCHINA A. , LOPEZ S. , BENITO M. 
Published: April 2006

SummaryBackground
Allergy to both house dust and storage mites is well established, but information about other species of mites is seant.Objective
One hundred and fifty patients directly exposed to an occupational environment were studied to assess whether spider mites (Tetranychidue) caused their allergic symptoms. We also studied a group of 50 patients from an urban environment, who were not occupationally exposed to spider mites, with a strong sensitization to Dermatophagoides pteronyssinus (RAST class 4).Methods
Case history (including questions about work‐related symptoms), skin tests, RAST and conjunctival provocation tests were performed in both groups using Tetranychus urticae and Panonychus citri extracts as allergens. Cross‐reactivity between spider mites and D. Pteronyssinus was determined by RAST inhibition.Results
Fifty‐four of 150 rural workers were positive to Tetranychidae and in all cases there was an associated sensitization to D. pteronyssinus. All individuals belonging to the urban group were positive to spider mites. RAST inhibition demonstrated a significant cross‐reactivity between Tetranychidae and D. pteronyssinus. Five of fifty‐four rural workers sensitized to spider mites developed symptoms only when they handled plants or fruits infested with spider mites and they became asymptomatic when exposure ceased.Conclusion
In the rural population studied. 36% of workers were found to be sensitized to spider mites and 10% had symptoms associated with occupational exposure. Since specific IgE antibodies to spider mites could not be detected in the absence of the specific IgE antibodies to D. pteronyssinus, and as all the affected workers were RAST positive to D. pteronyssinus, prior sensitization to house dust mites may be a risk factor for occupational allergy to spider miles.
Cytokine production in children outgrowing hen egg allergy
Authors: NOMA T. , YOSHIZAWA IZUMI , AOKI K. , YAMAGUCHI K. , BABA M. 
Published: April 2006

SummaryBackground
Approximately 40 to 80% of egg‐allergic children outgrow egg allergy after 2 to 5 years.Objective and methods
To detail the immunologic mechanisms involved in the development of tolerance to egg proteins, the bahince between interleukin 4 (IL4) and interferon‐γ (IFN‐γ) synthesis in patients with active atopic dermatitis allergic to hen egg and in those outgrowing hen egg allergy was evaluated.Results
A marked increase in IL4 and a decrease in IFN‐γ synthesis by peripheral blood lymphocytes following ovalbumin (OVA) specific in vitro stimulation was observed in active atopic dermatitis. In contrast, OVA‐induced IL4 synthesis in patients in remission was comparable to that in normal individuals. An intriguing finding was higher production of IFN‐γ by lymphocytes from ovalbumin‐inscnsitive patients in remission as compared to normal individuals following antigen stimulation. although cell proliferation in OVA‐stimulated lymphocytes was reduced in patients during remission.Conclusion
OVA antigen may be capable of inducing a population of Thl‐type cells to produce cytokines such as IFN‐γ, resulting in suppression of Th2‐type responses, i.e. IL4 secretion. We speculate that the changes in the balance of relevant antigen‐induced cytokine synthesis seen in such patients may be causally associated with the improvement in their clinical status.
Isotypic analysis of grass pollen‐specific antibodies in human plasma. 4. Biological activity of allergen‐specific and autoanti‐IgE antibody fractions on basophil histamine release
Authors: BATARD T. , WEYER A. , LAROZE A. , ICKOVIC M.‐R. , DAVID B. , PELTRE G. , BASUYAUX B. 
Published: April 2006

SummaryBackground
Blocking antibodies are defined as antibodies that compete with IgE for binding to allergens due to their specificity for those allergens. Thus, they may inhibit allergen‐induced basophil and mast cell IgE‐dependent mediator release both in vivo and in vitro.Objective
The present study was designed to evaluate the ability of antibodies isolated from human plasma samples on a Dactylis glomerata (Cocksfoot) pollen affinity‐column to inhibit the Dactylis pollen‐induced histamine release from human basophils (BHR) in vitro.Methods
Antibodies from Ig pools containing either high or low IgG4 anti‐Dactylis pollen were purified on a Dactylis pollen affinity‐column and then separated on an anti‐human Igl column. Obtained Ig fractions were incubated for 30 min with Dactylis pollen allergens prior to incubation with basophils from Dactylis pollen‐allergic donors. Cell supernatants were assessed for histamine content and the inhibition of BHR was calculated.Results
Unlike control non‐isolated Igs, the antibodies isolated on the Dactylis pollen column were able to inhibit efficiently and in a dose‐dependent manner Dactylis pollen‐induced BHR. The inhibitory activity was increased in isolated antibody samples that had high Ig(i4 levels. Antibodies isolated on the Dactylis pollen column, however, consisted not only of true allergen‐specific (potentially blocking) antibodies but also of autoanti‐Igl‐ binding to allergen‐specific IgE and mistaken for allergen‐specific antibodies, thus opening to question the involvement of the true allergen‐specific antibodies in the BHR‐inhibitory activity. Unlike the true allergen‐specific antibodies, the autoanti‐Igl were retained on and eluted from the anti‐lgF column. Results showed that both the autoanti‐IgE‐depleted and the autoanti‐IgF‐containing fractions accounted for the inhibition observed with the related non‐depleted sample that had been isolated on the Dactylis pollen column.Conclusion
For the first time, the true blocking activity of allergen‐specific antibodies is demonstrated, that is. in the absence of the autoanti‐Igl which can also inhibit BHR.
Glutathione‐S‐transferase induces murine dermatitis that resembles human atopic dermatitis
Authors: HSU CHING‐HSIANG , CHUA KAW‐YAN , HUANG SHAU‐KU , CHIANGI I‐PING , HSIEH KUE‐HSIUNG 
Published: April 2006

SummaryBackground
The molecular and functional basis of allergen‐induced inflammation seen in atopic dermatitis (AD) remains undefined.Objective
The objective of this study is to establish a murine model to dissect the pathological mechanisms of inflammatory reactions leading to the development of AD.Methods
An inbred strain of mice. BALB/c, when injected peritoneally with 30 μg of recombinant Sj26 protein (rSj26). a glutathione S‐transferase of Schistosoma japonicum worm, developed systematic dermatitis 21 days after immunization. The pathology of the dermatitis was examined by histological evaluation and immunostaining. The immediate skin hypersensitivity was demonstrated by scrum transfer and skin test. Epicutaneous patch test was used to demonstrate the antigen‐specific late phase response.Results
Significant responses of rSj26‐specific IgE were detected 2 weeks after immunization., and such changes paralleled formation of skin lesions. The diseased skin pathology showed inflammatory changes such as infiltration of mononuclear cells and eosinophils in the dermis and mild spongiosis in the epidermis. Numerous IgE bearing cells were also detected in the dermis. Peripheral blood showed eosinophilia at the same time. In addition, rSj26‐specific positive skin test and epicutaneous patch test could be demonstrated in rSj26‐sensitized mice.Conclusions
These results suggest that rSj26 is capable of eliciting atopic dermatitis‐like lesions in BALB/c mice. This can be a useful animal model for elucidating allergen‐induced immune responses and the development of various therapeutic interventions of atopic dermatitis in humans.
Comparison between hypertonic and isotonic saline‐induced sputum in the evaluation of airway inflammation in subjects with moderate asthma
Authors: BACCI E. , CIANCHETTI S. , PAGGIARO P. L. , CARNEVALI S. , BANCALARI L. , DENTE F. L. , DI FRANCO A. , GIANNINI D. , VAGAGGINI B. , GIUNTINI C. 
Published: April 2006

SummaryBackground
Hypertonic saline‐indueed sputum has recently been used for the evaluation of airway inflammation in asthma.Objective
To assess the effect of hypertonicity on airway inflammation.Methods
We compared the inflammatory cell composition of hypertonic saline‐induced sputum with that of isotonic saline‐induced sputum in 21 asthmatic subjects and, at baseline and 30min after each sputum induction, we measured bronchial hyper‐responsiveness to methacholine as an indirect marker to detect increased airway inflammation. On two different days, the patients inhaled hypertonic saline (3–5% NaCl) or isotonic saline (0.9% NaCl) for 30 min via an ultrasonic nebulizer, while monitoring FEV1. Sputum was collected for inflammatory cell analysis.Results
There was no difference in inflammatory cell percentages obtained with the two methods. Eosinophils were >1% in 20 subjects after hypertonic saline and in 16 subjects after isotonic saline, but this difference was not statistically significant. Intraclass correlation coefficients for sputum inflammatory cells obtained with the two methods were +0.642 for eosinophils, +0.644 for neutrophils. +0.544 for lymphocytes and +0.505 for macrophages. Hypertonic saline induced bronchoconstriction in a significantly greater number of subjects than isotonic saline. Also, hypertonic saline increased bronchial responsiveness to methacholine. while isotonic saline did not.Conclusion
We conclude that hypertonicity does not affect sputum cell composition, suggesting that inflammatory cells in hypertonic saline‐induced sputum are probably preexisting and not acutely recruited in the airways by the hypertonic stimulus. However, the bronchoconstriction and the increase in bronchial hyper‐responsiveness after hypertonic saline inhalation may imply the release of inflammatory mediators. This fact must be considered in the evaluation of soluble markers of inflammation in hypertonic salineinduced sputum.
Comparison between two automated systems to determine specific IgE: CAP and ELItest
Authors: BRUNNÉE T. , SEEBERGER A. , KLEINE‐TEBBE J. , KUNKEL G. 
Published: April 2006

SummaryBackground and objective
The ELItest® is a newly developed system to measure specific IgE based on allergen bound to paper rings and an alkaline phosphatase conjugated second antibody detection system. It was compared to the CAP® system, a method based on allergen conjugated to an encapsulated cellulose polymer and a β‐galactosidase conjugated fluorescence detection system.Methods
Sera of 300 patients with positive history and positive skin‐prick tests to common allergens (birch, timothy‐grass, cat dander, dermatophagoides pteronyssinus, wasp venom) and 30 negative controls were tested in both systems. Serial dilutions of high titre sera were measured; inter‐ and intraassay coefficients of variation (cv) were determined.Results
The CAP system proved to be more sensitive (92.3%) compared to ELItest (84%) but marginally less specific (94.7% for CAP versus 96.7% for ELItest). Intraassay cv were slightly lower in the ELItest (7.2% CAP versus 6.4% ELItest), whereas the interassay cv was roughly twice as high for ELItest (20.1%) than for the CAP system (11.4%). Linearity over an 8‐fold dilution was good in both tests (r2 0.979 ELItest versus 0.996 CAP), although ELItest levelled off at higher allergen concentrations. Similarly, correlation analysis between both systems revealed that ELItest consistently measured lower values, especially at higher concentrations of specific IgE. The slope of the linear regression line of a log/log plot of measured IgE concentrations was significantly lower than 1 in birch, cat and wasp; the y‐intersect was significantly lower than 0 in all analysed allergens.Conclusion
These results suggest that the ELItest system for the measurement of specific IgE is not quite as reproducible and sensitive as the CAP system but slightly more specific, and that higher concentrations of specific IgE are measured lower in the ELItest. One potential reason might be that the amount of allergen bound to a paper ring might be smaller than that bound to a cellulose polymer, but further experiments are necessary to prove this hypothesis.
Role of sensory neuropeptides in post‐allergic propranolol‐induced bronchoconstriction in guinea pigs in vivo
Authors: FUJIMURA M. , TSUJIURA M. , MYOU S. , ISHIURA Y. , MATSUDA T. 
Published: April 2006

SummaryBackground
Administration of propranolol can provoke bronchoconstriction in asthmatic patients. We hypothesized that such bronchoconstriction may result from the inflammatory mediators released by an allergic reaction. We recently developed a guinea pig model for propranolol‐induced bronchoconstriction (PIB). Neuropeptides which are released from C‐fibre nerve endings have been postulated to induce bronchial hyperresponsiveness through neurogenic inflammation.Objective
The purpose of this study was to examine whether sensory neuropeptides are involved in the development of PIB after allergic reaction.Methods
Propranolol at a concentration of 10mg/ml was inhaled 20min after antigen challenge in passively sensitized, anaesthetized and artificially ventilated guinea pigs. The animals were treated intravenously with a NK1 and NK2 dual antagonist, FK224, in a dose of 1 or 10 mg/kg or vehicle or a selective NK1 antagonist, FK888, in a dose of 1 or 10mg/kg or vehicle 10min before or 15min after antigen challenge.Results
Propranolol inhaled 20 min after antigen challenge caused bronchoconstriction. FK224 or FK888 administered 15 min after antigen challenge as well as 10 min before antigen challenge did not reduce the PIB.Conclusion
We conclude that neuropeptides such as neurokinin A and substance P do not directly contribute to the development of PIB after allergic reaction.
Increased numbers of dendritic cells in the bronchial mucosa of atopic asthmatic patients: downregulation by inhaled corticosteroids
Authors: MÖLLER G. M. , OVERBBEK S. E. , VAN HELDEN‐MEEUWSEN C. G. , VAN HAARST J. M. W. , PRENS E. P. , MULDER P. G. , POSTMA D. S. , HOOGSTEDEN H. C. 
Published: April 2006

SummaryBackground
Dendritic cells (DC) are the most potent antigen‐presenting cells (APC) and stimulators of T cells. Dendritic cells are also likely to be essential for the initiation of allergic immune responses in the lung. However, there are not many data on the presence of dendritic cells in the airways of patients with atopic asthma and on the effects of corticosteroid‐treatment on such dendritic cells.Objective
We investigated the distribution of dendritic cells in the bronchial epithelium and mucosa of 16 non‐smoking atopic asthmatic patients and eight healthy control subjects using detailed immunohistochemistry (CD l a, HLA‐DR, L25 as markers for dendritic cells).Methods
Eleven asthmatics were treated for 2.5 years with bronchodilators only and five with bronchodilators and inhaled beclomethasone dipropionate (BDP), 800 μg daily. The patients were randomly sampled from a double‐blind multicentre study. Results There were higher numbers of CD la+ DC (P = 0.003), L25+ DC (P = 0.002) and HLA‐DR expression (P = 0.042) in the bronchial mucosa of asthmatic patients compared with healthy controls. After 2.5 years of treatment, we found a significant increase in fiow expiratory volume in I second (FEV1) (P = 0.009) and a significant decrease in hyperresponsiveness (PC20 histamine) (P= 0.013) in the corticosteroid group (n = 5) compared with the bronchodilator group (n= 11). This dinical improvement in the corticosteroid‐treated group was accompanied by significantly lower numbers of CDla+ DC (P = 0.008), and HLA‐DR expression (P‐ 0.028) in the bronchial mucosa than in the bronchodilator‐treated group.Conclusion
Our data suggest that dendritic cells are involved in asthmatic inflammation and that corticosteroids may downregulute the number of dendritic.
Function and regulation of FcεRI expression on monocytes from non‐atopic donors
Authors: REISCHL I. G. , CORVAÍA N. , EFFENBERGER F. , WOEFF‐WINISKI B. , KRÖMER E. , MUDDE G. C. 
Published: April 2006

SummaryBackground
The high affinity receptor for IgE (FcεRI) has recently been identified on antigen presenting cells, i.e. Langerhans cells and monocytes from atopic donors and it was hypothesized that FcεRI expression levels correlated with allergy.Objective
The aims of the study was to investigate the function and expression of FcεRI on monocytes frotn non‐atopic donors.Methods
Purified monocytes or peripheral blood mononuclear cells were used to study FcεRI expression and signal transduction on CD14 positive cells by flow cytometry and/or confocal laser microscopy.Results
Freshly isolated monocytes from healthy individuals (n = 58) were shown to express FcεRI (median 18%, range 2–66%). No IgE was bound to these receptors in vivo, and in vitro no significant binding of complete IgE molecules could be obtained. IgE positive monocytes from atopic donors were also found to have free FcεRI, incapable of binding IgE in vitro. Oti all CD14 positive cells free FcεRI expression was rapidly and completely lost during culture in conventiotial culture media (IMDM. RPMI) but not in phosphate buffered saline (PBS). Moreover, signal transduction through free FcεRI appeared to be inhibited. However, both IgE binding and calcium mobilization were restored by treatment of fresh non‐atopic monocytes with neuraminidase. Importantly, culturing these monocytes overnight in conventional medium containing 2μg/mL IgE induced a cycloheximide insensitive accumulation of IgE bound to FcεRI and, in addition, led to cell activation.Conclusion
Monocytes from both atopic donors and healthy individuals express FcεRI, but the previously reported different expression levels between the two groups seem to be directly related to the absence or presence of TgE in the serum. This may be due to the fact that FcεRI is subjected to a constant turnover process which is slowed down but not prevented by ligand binding. In addition, free FcεRI on non‐atopic monocytes are under control of a neuramindase sensitive structure(s), which influences signal transduction and IgE binding.
Dendritic cells in normal and asthmatic airways: expression of the α subunit of the high affinity immunoglobulin E receptor (FcεRI‐α)
Authors: TUNON‐DE‐LARA J. M. , REDINGTON A. E. , BRADDING P. , CHURCH M. K. , HARTLEY J. A. , SEMPER A. E. , HOLGATE S. T. 
Published: April 2006

SummaryBackground
Immunoglobulin E (IgE) plays an important role in asthma, with total serum IgE levels closely related to both clinical expression of the disease and airway hyperresponsiveness. IgE binds to a high affinity cell‐surface receptor (FcεRI) which is present on mast cells and which has also recently been demonstrated on cutaneous dendritic cells. If pulmonary dendritic cells were also able to express this receptor, this would have important implications with regard to their potential role in asthma.Objectives
The aims of the study were to investigate the expression of the α subunit of the high affinity IgE receptor (FcεRI‐α) in normal and asthmatic airways, and to analyse its cellular provenance with particular emphasis on the dendritic cell.Methods
Bronchial biopsy specimens were obtained using fibreoptic bronchoscopy from 10 atopic asthmatics and nine non‐atopic non‐asthmatic control subjects. Specimens were processed into glycolmethacrylate resin and analysed by immunohistochemistry using specific monoclonal antibodies against FcεRI‐α. and against tryptase and CDla. markers for mast cells and dendritic cells, respectively.Results
The numbers of dendritic cells were significantly higher in the airways of asthmatics compared with those of control subjects (P<0.02). Analysis of sequential sections revealed that the α subunit of FcεRI was localized to both mast eells and dendritic cells. The proportion of dendritic cells expressing FcεRI‐α was significantly inereased in the asthmatic group (P < 0.003).Conclusion
These results support the hypothesis that dendritic cells play an important role in allergic asthma although the functional significance of FcεRI‐α expression needs further investigation.