bluuebunny/crossref_metadata_2025_split huggingface dataset:
Specific IgE antibodies to nickel in workers with known reactivity to cobalt
Authors: SHIRAKAWA T. , KUSAKA Y. , MORIMOTO K. 
Published: April 2006

SummaryTwenty‐one workers with hard metal asthma, including eight atopics, diagnosed on the basis of peak flow diaries and positive reaction to cobalt chloride (CoCl2) and/or nickel sulphate (NiSO4) in skin and provocation tests were studied for sensitization by detection of specific antibodies to nickel‐conjugated human serum albumin (Ni‐HSA), and nickel‐conjugated exchange resin (Ni‐resin). Their results were compared with those of sera obtained from control sera from 60 asthmatic patients and pair‐matched asymptomatic control workers in the hard metal plant. In the RASTs (radioallergosorbent tests), sera from the same six subjects developed positive reactions both to Ni‐HSA (RAST index > 2.0, P < 0.01) and Ni‐resin (RAST index > 2.0, P < 0.01), while the counts measured for the others of the 15 subjects (RAST index < 1.52) were about the same as those for control groups (RAST index < 1.58). Subject HSA RAST and resin RAST results (378.52 c.p.m. in HSA RAST and 324.56 in the resin RAST) were about the same as those of the control sera (388.65 c.p.m. and 398.59 c.p.m., respectively). There was no difference in the prevalence of smoking habit and high IgE between Ni‐RAST positive and negative subjects. However, subjects with simultaneous sensitivity to nickel and/or cobalt still developed asthmatic attacks following medications, while those without sensitivity to these metals were almost symptom free. The positive sera had simultaneous sensitivity to both cobalt and nickel, suggesting the presence in them of specific IgE antibodies to nickel playing some role in the aetiology of hard metal asthma.
Bronchial allergen challenge: dose versus concentration
Authors: FRØLUND L. , MADSEN F. , SCHARLING B. , HEINIG J. H. , SVENDSEN U. GERNER 
Published: April 2006

SummaryThis study was designed to investigate if two equivalent doses of allergen administered by different dosing regimes—two breaths and 10 breaths of each concentration—would result in the same magnitude of the early and late asthmatic response. Fifteen patients with extrinsic allergic asthma were challenged twice with either two or 10 breaths of twofold increasing allergen concentrations. The challenge was continued until a 20% decrease in FEV1 had been achieved. A non‐cumulative PC20FEV1 allergen was derived, and the cumulative dose of allergen given was similarly derived. In order to assess the reproducibility of the challenge, seven patients were challenged twice with two‐breath regime. The mean value of allergen PC20 obtained by the two‐breath regime was 4.1 fold (95% CI: 2.3–7.1 fold) greater than those obtained by the 10‐breath regime (P < 0.05), whereas the difference was 1.4 fold (95% CI: – 3.3–0.5 fold) for the cumulative dose (P > 0.05). A statistically significant larger magnitude of the early asthmatic response, as determined by the maximum per cent fall in FEV1, and late asthmatic response determined by the maximum per cent fall in peak expiratory flow domiciliary recorded during the following 24 hr after challenge, was observed in favour of the 10‐breath regime compared to the two‐breath regime (mean difference 6%, 95% CI: 0.6–11%). The reproducibility of the provocation test was acceptable (± 1.8 two‐fold concentration difference). These results confirm the ‘equivalent dose hypothesis’, and demonstrates that dosage rather than concentration appears to determine the early and late asthmatic response after bronchial allergen challenge.
Application of monoclonal antibodies against major basic protein (BMK‐13) and eosinophil cationic protein (EG1 and EG2) for quantifying eosinophils in bronchial biopsies from atopic asthma
Authors: MOQBEL R. , BARKANS J. , BRADLEY B. L. , DURHAM S. R. , KAY A. B. 
Published: April 2006

SummaryA monoclonal antibody prepared against the eosinophil major basic protein (MBP) was compared with the anti‐eosinophil cationic protein (ECP) antibodies (Eg1 and EG2) in immunostaining of bronchial biopsies from atopic asthma and controls. Anti‐MBP (designated BMK‐13) did not cross‐react with other eosinophil basic proteins (i.e. ECP, eosinophil peroxidase [EPO] or eosinophil‐derived neurotoxin [EDN]) and stained more than 98% of peripheral blood eosinophils irrespective of their degree of activation. EG2 stained 15% of resting and 75% of activated eosinophils; EG1 recognized 74% and 78% of resting and activated cells, respectively.The numbers of BMK‐13, EG1 or EG2‐positive staining cells in bronchial biopsies from asthma were significantly greater than atopic non‐asthmatics (P < 0.02, P < 0.01 and P < 0.05, respectively) and normal non‐atopic controls (P < 0.001). For each of the various groups studied, the rank order for the number of eosinophils stained was BMK‐13 > EG1 > EG2. BMK‐13 stained significantly more cells from bronchial biopsies of atopic asthma and atopic non asthma when compared to EG2(P < 0.001 and P < 0.05, respectively). Since only a proportion of BMK‐13+ cells were EG2+, these results suggest that not all tissue eosinophils are actively secreting. Thus, BMK‐13 can serve as a useful pan‐eosinophil marker in tissue sections since it appears to stain most eosinophils.
Specificity mapping of patients IgE response towards the tree pollen major allergens Aln g I, Bet v I and Cor a I
Authors: IPSEN H. , WIHL J.‐Å. , PETERSEN B. NÜCHEL , LØWENSTEIN H. 
Published: April 2006

SummaryThe specificity pattern of IgE from non‐treated tree pollen allergic patients (n= 38) were evaluated by solid phase absorption of serum samples followed by CRIE on alder, birch and hazel CIE precipitation profiles. The majority of the serum samples seemed to contain IgE antibodies with the following characteristics: specific towards Bet v I alone and common between Aln g I, Bet v I and/or Cor a I, ‘II’. The IgE specificity profiles observed for 95% of the sera tested are compatible with birch pollen allergens being the only sensitizing allergens, indicating that the patients react to allergens from other tree pollens of the Fagales order due to IgE cross‐reaction with the major allergens of birch and alder and/or hazel pollens.
Early neutrophil but not eosinophil or platelet recruitment to the lungs of allergic horses following antigen exposure
Authors: FAIRBAIRN S. M. , PAGE C. P. , LEES P. , CUNNINGHAM F. M. 
Published: April 2006

SummaryPrevious studies have shown that bronchoalveolar lavage fluid from horses with allergic respiratory disease and showing clinical symptoms contains increased numbers of neutrophils. In some cases, the eosinophil count is also increased. In this study the time course of changes in lung function and the accumulation of radiolabelled leucocytes and platelets in the lungs of allergic and normal horses has been examined during a 7 hr allergen exposure. Antigen challenge had no effect on pleural pressure or the distribution of radiolabelled neutrophils, eosinophils or platelets in normal horses. In contrast, in 6/8 allergic horses, there was an increase in pleural pressure and neutrophil accumulation in the lungs, both of which were evident after 4–5 hr. However, during the 7 hr challenge period radiolabelled eosinophils were detected in the lungs of only 1/6 horses exhibiting an increase in pleural pressure and in 1/7 horses that failed to show a change in airway function despite a clinical history of allergic respiratory disease. Antigen challenge did not alter the distribution of radiolabelled platelets in the five allergic horses tested. These results demonstrate that increased pleural pressure is not accompanied by eosinophil or platelet accumulation in the lungs of horses with allergic respiratory disease following exposure to antigen. However, changes in airway function can be associated with neutrophil accumulation but can also take place in the absence of this cell recruitment. This raises the possibility that the presence of neutrophils in the lung is not a prerequisite for changes in lung function.
Inhibition of bronchial hyperresponsiveness to histamine induced by intravenous administration of leukotriene C4 by novel thromboxane A2 receptor antagonists ONO‐NT‐126 and ONO‐8809 in guinea‐pigs
Authors: KUROSAWA M. , YODONAWA S. , TSUKAGOSHI H. 
Published: April 2006

SummaryWe studied the effect of intravenous administration of leukotriene (LT) C4 on bronchial responsiveness to histamine and airway wall thickening in guinea‐pigs. Guinea‐pigs were killed and the lungs were fixed in formalin. Slides from paraffin‐embedded sections of the lungs were stained and the airways that were cut in transverse sections were measured by tracing enlarged images using a digitizer. Moreover, airway resistance (Raw) was determined by a pulmonary mechanics analyser and we calculated two incides, an index of airway wall thickening and the one of airway hyperresponsiveness to histamine, from changes of baseline‐Raw and peak‐Raw following intravenous administration of histamine before and after the intravenous administration of LTC4. Intravenous administration of 3 μg/kg LTC4 for 1 hr induced an increase of the relative thickness of the airway wall in peripheral bronchi by the histological examination. In analysis of airway function, intravenous administration of 3 μg/kg LTC4 for 1 hr induced airway hyperresponsiveness to histamine with airway wall thickening. Thromboxane A2 receptor antagonists ONO‐NT‐126 and ONO‐8809 inhibited the LTC4‐induced airway hyperresponsiveness to histamine in a dose‐dependent manner, but not the airway wall thickening induced by LTC4, suggesting that the effect of LTC4 on bronchial hyperresponsiveness is likely to be mediated through TXA2.
Genetic polymorphism of the β‐2 adrenergic receptor in atopic and non‐atopic subjects
Authors: POTTER P. C. , VAN WYK L. , MARTIN M. , LENTES K. U. , DOWDLE E. B. 
Published: April 2006

SummaryTo investigate a possible genetic basis for reported differences in β‐2 receptor expression in atopic subjects, DNA from 42 atopic children (22 asthmatics and 22 with allergic rhinitis) and 30 non‐atopic subjects was Southern blotted and Ban‐1 restriction fragment polymorphisms (RFLPS) were studied using a 2.6 kb probe of the human β‐2 receptor gene. Two alleles 3.1 kb and 2.9 kb were identified. Homozygotes and heterozygotes for the two alleles were found with equal frequency in the atopic patients who had asthma and in those who had allergic rhinitis only. The gene frequencies for the upper and lower alleles were 0.45 and 0.55 respectively. Our studies do not provide evidence for an association between a particular polymorphic form of the human β‐2 receptor gene and atopy.
Atopy in childhood. I. Gender and allergen related risks for development of hay fever and asthma
Authors: SEARS M. R. , BURROWS B. , FLANNERY E. M. , HERBISON G. P. , HOLDAWAY M. D. 
Published: April 2006

SummaryReasons for the gender differences in prevalence rates for asthma remain unclear. We have examined the relationships between allergen skin‐test reactions and diagnoses of hay fever and asthma in New Zealand hoys and girls examined at the age of 13 years. Information on current and past wheezing, diagnosed asthma, and hay fever was obtained for 662 subjects (341 boys) of a birth cohort followed longitudinally to the age of 13 years, using a physician‐administered questionnaire. Atopic status was determined by skin‐prick tests to 11 common allergens. The proportion of 13‐year‐old boys with current asthma was 1.6 times higher and of ever‐diagnosed asthma 1.4 times higher than in girls, but the prevalence of recurrent wheeze ( three episodes per year) not diagnosed as asthma, or of hay fever, was not significantly different between the sexes. The prevalence of diagnosed asthma increased with increasing numbers of positive skin tests, but hay fever without asthma was little affected above one positive skin‐test. Boys had a greater prevalence of any positive skin‐test (50.1 % vs 37.1%), two or more positive tests (29.3 % vs 21.8%), and responses to house dust mite (34.0% vs 23.1 %) and cat (14.7% vs 11.2%). Gender differences for asthma became insignificant when adjusted for skin‐test responsiveness to house dust mite and/or cat. The proportion of children with diagnosed asthma increased with increasing size of weals to house dust mite and cat dander. Gender differences in allergen sensitivities partly explain the gender differences in diagnosed asthma in children. In both sexes, risk of asthma was primarily associated with sensitization to indoor allergens (house dust mite and cat), and was related to the magnitude of the skin‐test response, while the risk of hay fever was primarily associated with grass pollen sensitivity.
Atopy in childhood. II. Relationship to airway responsiveness, hay fever and asthma
Authors: SEARS M. R. , BURROWS B. , HERBISON G. P. , HOLDAWAY M. D. , FLANNERY E. M. 
Published: April 2006

SummaryWhile airway hyperresponsivencss is usually associated with a diagnosis of asthma or symptoms of wheezing, some individuals with rhinitis show airway hyperresponsiveness as do some with no symptoms whatsoever. We have studied the correlations between symptoms, airway hyperresponsiveness and atopy as determined by skin‐prick tests in a cohort of New Zealand children. A total of 662 members of a birth cohort were studied at age 13 years using a respiratory questionnaire, skin‐prick tests to 11 common allergens, and an abbreviated validated methacholine challenge test to determine airway responsiveness. Airway hyperresponsiveness (methacholine PC20 FEV1 8 mg/ml) was strongly correlated with reported asthma and current wheezing (P < 0.0001) and also with atopy, especially to house dust mite and cat (P < 0.0001). As weal size for both house dust mite and cat increased, so did the proportion of children with airway hyperresponsiveness. All children with diagnosed asthma and airway hyperresponsiveness were atopic. Skin‐test reactions to house dust mite and cat were strongly correlated with any degree of measurable airway responsiveness (PC20 FEV125 mg/ml) in children with rhinitis (P < 0.0001), and remained significantly correlated even in children without current asthma, without asthma ever and without rhinitis (P < 0.001). Atopy is a major determinant of airway hyperresponsiveness in children, not only in those with reported histories of asthma and wheezing, but also in the absence of any history suggesting asthma and rhinitis.
Peripheral blood mononuclear cells from house dust mite allergic patients produce IL‐2 in response to specific allergen challenge
Authors: MCHUGH S. M. , LACHMANN P. J. , EWAN P. W. 
Published: April 2006

SummaryProliferative responses and production of IL‐2 by peripheral blood mononuclear cells of patients with Dermatophagoitles pieronyssinus rhinitis ± asthma were measured at up to 24 hr intervals from 1–8 days, after stimulation with mitogen (PHA), antigen (SKSD) and specific allergen (D.pteronysxinus). IL‐2 was measured in culture supcrnaunts using the murine CTLL cell line bioassay. Compared to non‐atopic controls, patients had significantly higher prolilenitive responses to D. pteronyssinus and SKSD but similar responses to PHA. In patients, maximal proliferate responses to PHA, SKSD and D. piemnyxsinus were at 3, 6 and 7 days, respectively. IL‐2 levels in response to stimulation with D. pieronvssinus were significantly higher in patients than controls, where only background levels were found (15.4, 7.9–30.7− 10‐2 U/ml [mean, range] n=11;vs 2.2,0.1–8.4 × 10‐2 U/ml, n= 6; P< 0.05). In contrast, IL‐2 production to PHA and SKSD, although higher in patients, was not significantly different than controls. These results suggest allergic patients possess a population of T cells expandable by specific allergen which are induced to secrete IL‐2.
β2‐Adrenoceptor stimulation augments the IL‐4‐induced CD23 expression and release and the expression of differentiation markers (CD14, CD18) by the human monocytic cell line, U 937
Authors: PAUL‐EUGENE N. , DUGAS B. , GORDON J. , KOLB J. P. , CAIRNS J. A. , PAUBERT‐BRAQUET M. , MENCIA‐HUERTA J. M. , BRAQUET P. 
Published: April 2006

SummaryThe effect of β2‐adrenoceptor agonists and interleukin‐4 (IL‐4) on the CD23 expression on, and release from, the human promonocytic cell line, U 937, was investigated. As assessed by flow cytometry, incubation of U 937 cells in the presence of salbutamol, fenoterol or IL‐4 induced a concentration‐ and time‐dependent increase in CD23 expression, that was maximal after 48 hr and followed by a decrease thereafter. In addition, salbutamol potentiated the effect of IL‐4, the optimal concentration of the drug being a function of the concentration of this cytokine. This synergy between IL‐4 and β2‐adrenoceptor agonists was also observed for the release of the soluble form of CD23. The effect on CD23 expression of salbutamol and fenoterol, but not of IL‐4, was blocked in the Wesence of d, l‐propranolol (1 μm) or butoxamine (1 μm). The α‐adrenoceptor agonist, norepinephrine (1 μm), was ineffective in inducing CD23 expression or potentiating the one evoked by IL‐4. Salbutamol down‐regulated the expression of FcγRI (CD64) and Fc, RII (CD32) whereas IL‐4 was ineffective. Only when added together at the onset of the culture did salbutamol and IL‐4 induce, after 48 hr, the expression of the monocyte marker, CD 14. The expression of CD 18 was up‐regulated in response to salbutamol either alone or in combination with IL‐4, this cytokine alone being inefficient. These data suggest that IL‐4 and β2‐adrenoceptor agonists induce differentiation of U 937 cells into monocyte‐like cells.
Environmental exposure to Aspergillus fumigatus allergen (Asp f I)
Authors: SPORIK R. B. , ARRUDA L. K. , WOODFOLK J. , CHAPMAN M. D. , PLATTS‐MILLS T. A. E. 
Published: April 2006

Summary Asp f I is a major allergen produced by the mycelia of Aspergillus fumigatus. It is not present in spores and can be used as a specific marker for the detection of germination of this fungus. We investigated the domestic and outdoor concentration of Asp f I in Poole, U.K. and Charlottesville, VA, U.S.A. Asp f I was undetectable in 95% (281/296) of house dust extracts and present at low levels (< 0.17 μg/g of sieved dust, mean 0.038 μg/g) in the remainder. In contrast, Asp f I could be detected in 65% (15/23) of cultures of house dust, suggesting the presence of viable, but ungerminated, A. fumigatus in the majority of homes. Asp f I was detectable in 80% (28/35) of extracts of leaves and compost, but present in these outdoor samples at low levels (<0.11 μg/g, mean 0.27 μg/g). Air sampling for Asp f I was undertaken before and after vigorous disturbances at indoor (n= 5) and outdoor (n= 6) sites. Airborne Asp f I was not detected in domestic samples or in undisturbed outdoor samples. Following disturbance it could be measured in outdoor samples (range 7.6–29 ng/m3). The results suggest that while exposure to A. fumigatus is common, exposure to Asp f I and germinating A. fumigatus is uncommon. It is probable that those individuals who develop antibody responses to Asp f I have been exposed to A. fumigatus which has germinated in their respiratory tract.
Allergenicity of the cat flea (Ctenocephalides felis felis)
Authors: TRUDEAU W. L. , ÁNDEZ‐CALDAS E. FERN , FOX R. W. , BRENNER R. , BUCHOLTZ G. A. , LOCKEY R. F. 
Published: April 2006

SummaryAdult fleas, spent and unspent culture media were extracted and the radio‐atlergosor‐bent test (RAST) performed with sera of 48 cat flea skin test‐positive individuals from the Tampa Bay area of Florida. Sixteen sera (33.6%) had a positive RAST to the cat flea extract prepared in our laboratory [1.7‐11.4% of the total counts (TC) added]. Six of the 16 sera (12.5%) also contained specific IgE to allergens in thespent medium (0.8‐3.3% TC). The allergen composition and strength were studied by RAST inhibition of two commercial cat flea extracts and compared with our in‐house flea extract. The results demonstrated similar allergen compositions and different potencies. Sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS‐PAGE) of the in‐house flea extract showed several Coomassie blue‐stained bands (10–85 kD). SDS‐PAGE immunoblols revealed five IgE‐binding bands at 34, 35, 39, 54 and 60 kD. Flea allergens were quantified in eight house dust samples using RAST inhibition assays and expressed as RAST inhibition units; five of these samples contained detectable levels. Cat flea allergens may contribute to the allergenicity of house dust in areas of heavy llea infestation.
Cutaneous IgE‐mediated inflammatory lesion size is inhibited by an H1 antagonist (terfenadine) while mediator release is unaffected in vivo and in vitro
Authors: MASSEY W. A. , CHARLESWORTH E. N. , FREIDHOFF L. , COOPER P. , KAGEY‐SOBOTKA A. , LICHTENSTEIN L. M. 
Published: April 2006

SummaryWe are interested in understanding the pathogenesis of the cutaneous IgE‐mediated late phase reaction. A double‐blind, placebo‐controlled, randomized cross‐over study with 10 subjects of the effect of the non‐sedating antihistamine, terfenadine (Selddane), on the cutaneous reaction to antigen (ragweed or mixed grass) administered intradermally and over denuded blister bases was performed. The activity of terfenadine on anti‐IgE‐induced mediator release from the skin mast cell, lung mast cell and basophil was also examined in vitro. Terfenadine significantly inhibited the size of the cutaneous reaction at every hour between hours 1 and 9 (hr 9, control 2250 ± 500 mm2vs drug 1250 ± 250 mm2, P < 0.01, n=10) and showed some inhibitory effect at hours 10–12. While terfenadine blocks histamine release after nasal antigen challenge the release of mediators at skin blister sites was unaffected. The infiltration of leucocytes into the blister supernatant was unaffected by terfenadine although previous studies have shown significant inhibition with another antihistamine, cetirizine. In vitro, terfenadine. like other antihistamines, was found to have inhibitory activity on anti‐IgE‐induced mediator release at concentrations of 10−4‐10−5 M in lung and skin mast cells and basophils. We conclude that the effects of the newer antihistamines on cellular movement into the skin may be diverse, that terfenadine may show organ specificity in vivo and that terfenadine significantly decreases both the early and late gross inflammatory response of the skin to antigen. We cannot, as yet. explain the mechanism(s) by which this occurs.
A comparison of topical levocabastine and sodium cromoglycate in the treatment of pollen‐provoked allergic conjunctivitis
Authors: FROSTAD A. B. , OLSEN A. K. 
Published: April 2006

SummaryA total of 71 patients with documented birch and grass pollen allergy participated in this randomized, double‐blind, parallel‐group study initiated to compare the long‐term therapeutic efficacy of twice daily levocabastine, a new topical H1‐receptor blocker, with that of sodium cromoglycate four times daily in the treatment of pollen‐provoked conjunctivitis. There was no statistically significant difference in therapeutic efficacy between the two treatment groups, although a positive trend in favour of levocabastine was observed. Global evaluations of therapeutic efficacy were similar in both treatment groups. A total of 94% of levocabastine‐treated patients rated treatment to be excellent or good compared with 86% of patients in the sodium cromoglycate group. Moreover, there were no significant differences in the severity of allergic symptoms reported on the patient diary cards. Patients were permitted to use rescue medication (oral terfenadine and betamethasone nasal spray) if symptoms became severe. The use of rescue medication was lower in the levocabastine group than in the sodium cromoglycate group. The mean number of days on which rescue medication was used was 12.8 and 26.9 in the two groups, respectively. The incidence, and type, of adverse reactions was similar in both patient groups. Levocabastine is well‐tolerated and at least as effective as sodium cromoglycate in the treatment of pollen‐provoked conjunctivitis.