bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intestinal microbiota and immunoglobulin E responses in 5‐year‐old Estonian children
Authors: Sepp E. , Julge K. , Mikelsaar M. , Björkstén B. 
Published: September 2005

SummaryBackground
Over the last few decades, several studies from different parts of the world have indicated an increasing prevalence of allergic diseases. This has been related to environmental factors, like changes of microbial pressure. Our previous studies have demonstrated differences in the intestinal microbiota between allergic and non‐allergic children.Aim
To test the hypothesis that the intestinal microbiota and IgE response are related, both in allergic and non‐allergic 5‐year‐old Estonian children.Methods
The study group comprised 19 allergic and 19 non‐allergic 5‐year‐old children, selected from a larger group who had been followed from birth. The diagnosis of allergy was based on clinical examination of the children and on data obtained from the questionnaires. The faecal microbiota were quantified by seeding serial dilutions on nine different media for incubation in different environment. The composition of the gut microbiota was expressed both as absolute counts of the various species and their relative share among the total counts of identified microbiota.Results
Bifidobacteria were less commonly detected in children with allergic diseases than in healthy children and clostridia comprised a higher proportion among their gut microbes. Children with specific IgE antibodies to defined allergens had higher counts of clostridia and the counts of clostridia correlated with the level of serum IgE, but only so in allergic children. In non‐allergic children, the serum IgE levels showed a positive correlation with the counts of bacteroides.Conclusion
The development of allergic diseases seems to be associated with the composition of the gut microbial ecosystem. High counts of potential pathogens, such as clostridia, are associated with clinical manifestations of allergy and IgE antibody formation.
Diagnosing immediate reactions to cephalosporins
Authors: Romano A. , Guéant‐Rodriguez R.‐M. , Viola M. , Amoghly F. , Gaeta F. , Nicolas J.‐P. , Guéant J.‐L. 
Published: September 2005

SummaryBackgroundAfter penicillins, cephalosporins are the betalactams that most often induce IgE‐mediated reactions. The development of diagnostic tests has been delayed, however, because the cephalosporin allergenic determinants have not been properly identified.ObjectiveTo evaluate the usefulness of skin tests, serum specific IgE assays, and challenges in diagnosing immediate reactions to cephalosporins and to clarify the pathogenic mechanism of such reactions.MethodsWe studied 76 adults with immediate reactions to cephalosporins, mainly ceftriaxone, cefotaxime, and ceftazidime. Skin tests and serum specific IgE assays were performed for culprit cephalosporins and cefaclor, as well as for penicillin, amoxicillin, and ampicillin. Some subjects with negative results underwent challenges and re‐evaluations. Responses to cephalosporins other than the culprit ones were also studied.ResultsIn the first allergologic work‐up, an IgE‐mediated hypersensitivity to penicillins and/or cephalosporins was diagnosed in 63 (82.9%) of the 76 patients on the basis of skin‐test and/or specific IgE assay positivity. Of the 13 negative patients, eight accepted challenges and underwent re‐evaluations. Considering both first‐ and second‐evaluation results, the skin‐test‐positivity rate increased from 76.3% to 85.5% and that of sepharose‐radioimmunoassay positivity from 67.1% to 74.3%. Overall, an IgE‐mediated hypersensitivity was diagnosed in 70 patients (in seven after retesting). On the basis of skin‐test and CAP‐FEIA results, we classified our 76 patients into five groups: group A (three patients), positive only to penicillin reagents; B (17), positive to both cephalosporin and penicillin reagents; C (24), positive to more than one cephalosporin; D (21), positive only to the responsible cephalosporin; E (11) negative to skin tests and CAP‐FEIA, including five sepharose‐radioimmunoassay positive.ConclusionsMost immediate reactions to cephalosporins appear to be IgE‐mediated. Cephalosporin skin testing and sepharose‐radioimmunoassay are useful tools for evaluating these reactions. Cephalosporin IgE‐mediated hypersensitivity may be a transient condition; therefore, allergologic exams should be repeated in patients with negative initial allergologic work‐ups, including challenges.
Effect of salbutamol on nasal symptoms and mast cell degranulation induced by adenosine 5′ monophosphate nasal challenge
Authors: Russo C. , Zeng D. , Prosperini G. , Spicuzza L. , Guarino F. , Polosa R. 
Published: September 2005

SummaryBackground
In addition to its well‐known functional agonism at the level of β2 adrenergic receptors on airways smooth muscle cells, salbutamol appears to have additional protective effects, possibly through an inhibition of mast cell activation.Objective
The aim of this study is to provide the first evidence in vivo of inhibition of human mast cell activation by salbutamol.Methods
Nine atopic subjects received placebo and salbutamol (5 mg/mL) 15 min before an adenosine 5′ monophosphate (AMP) nasal provocation in a double‐blind crossover study design. The nasal lavage was collected from these subjects prior to or 3, 5, 15 or 30 min after the AMP nasal challenge, and concentrations of histamine and tryptase in the nasal lavage were measured.Results
AMP nasal provocation produced considerable sneezing and induced a transient increase in histamine and tryptase release with peak values achieved at 3 min after the challenge in all the subjects studied. Compared with placebo, salbutamol significantly attenuated the release of histamine and tryptase induced by AMP challenge (P=0.048 and 0.020, respectively). Moreover, the AMP‐induced sneezing was also inhibited by pre‐treatment with salbutamol (P=0.004).Conclusions
Intranasal salbutamol attenuates nasal symptoms and inhibits histamine and tryptase release caused by AMP nasal provocation thus supporting the hypothesis that salbutamol may play an additional protective role in the airways by inhibiting mast cell activation.
Association between bronchodilating response to short‐acting β‐agonist and non‐synonymous single‐nucleotide polymorphisms of β2‐adrenoceptor gene
Authors: Cho S.‐H. , Oh S.‐Y. , Bahn J.‐W. , Choi J.‐Y. , Chang Y.‐S. , Kim Y.‐K. , Min K.‐U. , Kim Y.‐Y. 
Published: September 2005

SummaryBackground
With β‐agonists being the most widely used agents in the treatment of asthma, in vitro studies reported that β2‐adrenergic receptor (ADRB2) polymorphisms are associated with agonist‐promoted down‐regulation.Objective
The present population‐based study aimed to evaluate the association between bronchodilating response to inhaled short‐acting β‐agonist and two non‐synonymous single‐nucleotide polymorphisms (SNPs) of ADRB2 (ADRB2‐16 and ADRB2‐27).Methods
Two hundred and nine children with reduction in forced expiratory volume in 1 s of more than 20% on methacholine bronchial challenge underwent bronchodilating response testing 5 min after the inhalation of 200 μg of albuterol. Of these 209, 195 gave peripheral blood for genotyping of ADRB2 polymorphisms.Results
The bronchodilating response was significantly higher in subjects with the homozygous Arg16 than in those with the homozygous Gly16. It was further demonstrated that haplotype pairs of the homozygous Arg16Gln27 and of the heterozygous Arg16Gln27/Gly16Glu27 showed the highest bronchodilating responses, and the haplotype pairs of the homozygous Gly16Gln27 the lowest response. As a whole, the bronchodilating response was more positively associated with the combined quantity of Arg16 and Glu27 polymorphisms than with that of Arg16 alone.Conclusion
Non‐synonymous SNPs of ADRB2 at codons 16 and 27 is significantly associated with bronchodilating response to inhaled short acting β‐agonists.
l‐Selectin expression on neutrophils from allergic patients
Authors: Monteseirín J. , Chacón P. , Vega A. , Sánchez‐Monteseirín H. , Asturias J. A. , Martínez A. , Guardia P. , Pérez‐Cano R. , Conde J. 
Published: September 2005

SummaryBackground
L‐selectin (CD62L) is an adhesion molecule involved in leucocyte attachment to endothelium at sites of inflammation, and it has been demonstrated that L‐selectin is rapidly shed after neutrophil activation. Recently, it has been reported that there is increasing evidence of neutrophil participation in asthma and the allergic process.Objective
The present study was designed to determine whether an IgE‐dependent mechanism can modulate L‐selectin expression on the surface of neutrophils. Moreover, we analyse the potential implication of intracellular signal‐transduction pathways and whether specific immunotherapy (IT), glucocorticoids and antihistamines might regulate this process.Methods
Peripheral blood neutrophils from three groups of donors (asthmatic group without IT treatment, IT‐treated asthmatic group and healthy group) were used. Cells were challenged in vitro with the specific allergen that produced clinical symptoms in asthmatic patients and also with the allergen to which the patients were not sensitive. Neutrophils from healthy donors were also challenged with allergens. Expression of CD62L on the neutrophil surface was analysed by flow cytometry, and soluble CD62L (sCD62L) in culture supernatant by ELISA. In an attempt to discover which IgE receptor is involved, we also challenged the neutrophils with monoclonal antibody to FcɛRI, FcɛRII (CD23) and galectin‐3 receptors.Results
When neutrophils from allergic patients were challenged with specific allergens that produce clinical allergy symptoms, L‐selectin was down‐regulated from the surface of those cells, accompanied by a concomitant up‐regulation of soluble L‐selectin in the supernatant. The challenge with antibodies against FCɛRI, FCɛRII (CD23) and galectin‐3, induces down‐modulation of L‐selectin on the surface of the neutrophils in all three cases. Calphostin C, wortmannin and manoalide attenuated CD62L down‐regulation, suggesting the potential implication of protein kinase C, phosphatidylinositol 3‐kinase and phospholipase A2 in the process. IT and glucocorticoids modulated allergen‐dependent CD62L down‐regulation, whereas antihistamines (terfenadine, loratadine and cetirizine) or nedocromil sodium did not affect the shedding of L‐selectin.Conclusions
We present evidence that the neutrophil surface expression of CD62L can be modulated by an allergen‐dependent mechanism. The modulation of CD62L expression can be induced through the three receptors of IgE. This process can be affected by IT.
Dendritic cells in asthma: a function beyond sensitization
Authors: Van Rijt L. S. , Lambrecht B. N. 
Published: September 2005

SummaryAllergic asthma is one of the most common chronic diseases in western society, characterized by variable airway obstruction, mucus hypersecretion and infiltration of the airway wall with T‐helper type 2 (Th2) cells, eosinophils and mast cells. If we are to devise new causal therapies for this disease, it is important to elucidate how Th2 cells are activated and respond to intrinsically harmless allergens. Dendritic cells (DCs) are the most important antigen‐presenting cells in the lung and are mainly recognized for their exceptional potential to generate a primary immune response and sensitization to aeroallergens. Much less attention has been paid to the role of DCs in established inflammation. Based on functional studies in a murine model for asthma, in this review article, we propose that DCs are essential for generating allergen‐specific effector Th2 responses in ongoing inflammation in sensitized mice. A better understanding of the role of DCs in the maintenance of the inflammatory response to allergens in asthma should lead to new therapeutic approaches intervening at the top of the inflammatory cascade.
Increased interferon‐γ‐ and interleukin‐4‐synthesizing subsets of circulating T lymphocytes in pregnant asthmatics
Authors: Tamási L. , Bohács A. , Pállinger É. , Falus A. , Rigó J. , Müller V. , Komlósi Z. , Magyar P. , Losonczy G. 
Published: September 2005

SummaryBackground
Pregnancy frequently interferes with the course of bronchial asthma, and asthmatic pregnant women experience less successful pregnancies. T lymphocytes synthesizing IL‐4 or IFN‐γ are important in allergic mechanisms of the airways as well as in materno‐fetal immunity.Objective
We hypothesized that pregnancy (a T helper‐2 polarized state) of asthmatics will enhance the number of circulating T2 lymphocytes, but decrease the subset‐producing IFN‐γ (T1 lymphocytes) and thereby cause a culminating T2 dominance with possible clinical consequences.Methods
IL‐4‐ or IFN‐γ‐producing T lymphocytes were determined by flow cytometry in healthy (n=8) and asthmatic (n=13) non‐pregnant women and healthy (n=18) and asthmatic (n=48) pregnant women of similar chronological and gestational (2nd–3rd trimester) age and asthma severity (Global Initiative for Asthma II–III).Results
In the blood of non‐pregnant women – healthy or asthmatic – the numbers of IL‐4‐ and IFN‐γ+ T cells were very low (<10/μL blood). In contrast, in asthmatic pregnant women, the cell counts were 182±27 and 39±6 for IFN‐γ+ and IL‐4+ T cells/μL blood, respectively (both P<0.05 vs. respective control values of non‐pregnant asthmatics). Within the asthmatic pregnant group, significant negative correlations were revealed between the numbers of IFN‐γ+ or IL‐4+ T cells and maternal peak expiratory flow as well as birth weight of newborns (both P<0.05).Conclusion
These data show a previously unknown immunological interference between asthma and pregnancy. The culminating proliferation of IFN‐γ+ and IL‐4+ T lymphocytes may potentially impair maternal airway symptoms as well as fetal development.
Cysteinyl leukotrienes induce monocyte chemoattractant protein 1 in human monocytes/macrophages
Authors: Ichiyama T. , Hasegawa M. , Ueno Y. , Makata H. , Matsubara T. , Furukawa S. 
Published: September 2005

SummaryBackground
Monocytes/macrophages have a cysteinyl leukotriene 1 (CysLT1) receptor, but its function is poorly understood.Objective
To elucidate the biological function of the CysLT1 receptor of human monocytes/macrophages.Methods
We examined the production of TNF‐α, IL‐1β, IL‐2, IL‐4, IL‐6, IL‐8, IL‐10, monocyte chemoattractant protein 1 (MCP‐1), macrophage colony‐stimulating factor (M‐CSF), and eotaxin induced by CysLTs (leukotriene (LT)C4, ‐D4, and ‐E4) in THP‐1 cells, a human monocytic leukaemia cell line, and peripheral blood CD14+ monocytes/macrophages. Moreover, we examined the effect of CysLTs on the expression of β‐chemokine receptor 2B (CCR2B) as the receptor of MCP‐1 by Western blot analysis.Results
ELISA revealed that CysLTs induced MCP‐1 in THP‐1 cells and peripheral blood CD14+ monocytes/macrophages, but not other cytokines. PCR demonstrated that CysLTs increased MCP‐1 mRNA expression in THP‐1 cells, and Western blotting showed that CysLTs increased the expression of CCR2B in THP‐1 cells. Moreover, we demonstrated that pranlukast, a CysLT1 receptor antagonist, blocked MCP‐1 production by CysLTs in THP‐1 cells almost completely, and partially inhibited MCP‐1 release by CysLTs in peripheral blood CD14+ monocytes/macrophages and CCR2B expression by CysLTs in THP‐1 cells.Conclusion
CysLTs induce MCP‐1 and increase CCR2B expression in human monocytes/macrophages.
Inflammatory mediators in exhaled breath, induced sputum and saliva
Authors: Simpson J. L. , Wood L. G. , Gibson P. G. 
Published: September 2005

SummaryBackground and Objective
Airway inflammation is assessed to monitor progression, control and treatment of asthma. The collection of exhaled breath condensate (EBC) provides a non‐invasive alternative to induced sputum samples for the monitoring of airway inflammation. Both samples can be confounded by salivary contamination. The aim of this study was to compare the levels of inflammatory mediators in samples of EBC, induced sputum and saliva samples from subjects with asthma.Method
EBC, saliva and induced sputum samples were collected from subjects with asthma (n=10). Total protein, IL‐8, 8‐isoprostane and surfactant protein A (SPA) were assessed in each sample.Results
Total protein, IL‐8, 8‐isoprostane and SPA were detected in all sputum samples. Only total protein and SPA were consistently measured in EBC, with levels at least 100‐fold lower than those measured in induced sputum. In saliva, total protein, SPA and 8‐isoprostane were detected in all samples, with IL‐8 detected in 60% of samples.Conclusions
Induced sputum is a reliable technique that can be used to assess markers of airway inflammation. While EBC is a simple and inexpensive technique to collect lower airway secretions, the detection of inflammatory mediators is variable, and further work is required to validate this technique to assess inflammatory mediators.
Perinatal characteristics and obstetric complications as risk factors for asthma, allergy and eczema at the age of 6 years
Authors: Bernsen R. M. D. , De Jongste J. C. , Koes B. W. , Aardoom H. A. , Van Der Wouden J. C. 
Published: September 2005

SummaryBackground
Considerable effort has been put into identifying early determinants for atopic disorders. Many studies have evaluated the role of fetal development and obstetric complications. However, the results are not unequivocal.Study objective
To assess the relationship between perinatal characteristics and obstetric complications, and the presence of reported current asthma, allergy and eczema at the age of 6 years in the framework of a previously conducted study.Method
Seven hundred families in the Netherlands with index children born in 1988–1990 were retrospectively selected. Data were extracted from the Municipal Health Service's records of health examinations of these children and their siblings. These examinations were carried out at the age of 6 years. The records contained data on reported atopic disorders and perinatal characteristics.Results
Gestational age was inversely related to the risk of asthma (P for trend: 0.03). Children with low birth weight tended to have a lower risk of any allergy, albeit not significant (P=0.07). However, no link was found between neonatal head circumference and atopic disorders. The ratio of neonatal head circumference to birth weight was positively associated with the risk of atopic disorders, especially with the risk of asthma (odds ratio (OR)=1.87; 95% confidence interval (CI95%)=[1.11, 3.15]).Vacuum extraction was a risk factor for allergy (OR=1.84, CI95%=[1.03, 3.28]), but not for asthma. Induced labour was positively associated with the risk of inhalant allergy (OR=2.22, CI95%=[1.09, 4.51]) and, to a lesser extent, asthma (OR=1.72, CI95%=[0.95, 3.10]). For caesarean section and forcipal extraction there were no such relationships.Conclusions
Prematurity is a risk factor for asthma reported at 6 years. A high ratio of head circumference to birth weight is a risk factor for any atopic disorder. Vacuum extraction was associated with a higher risk of allergy, and induced labour is a risk factor for inhalant allergy. All results should be viewed with the possibility of residual confounding.
Juvenile chinook salmon (Oncorhynchus tshawytscha) growth on the central California coast during the 1998 El Niño and 1999 La Niña
Authors: BRUCE MACFARLANE R. , RALSTON STEPHEN , ROYER CHANTELL , NORTON ELIZABETH C. 
Published: September 2005

AbstractWe assessed growth in subyearling chinook salmon (Oncorhynchus tshawytscha) during the 1998 El Niño and 1999 La Niña in the Gulf of the Farallones, a region of the continental shelf off central California seaward of the Golden Gate and the southernmost ocean entry point for the species in North America. Juvenile salmon demonstrated greater growth during this strong El Niño, when water temperature anomalies of more than +3°C were recorded at local buoys, than during the similarly strong 1999 La Niña. Slopes of regressions of weight on length, length on age, and weight on age were all significantly greater for juvenile salmon during the 1998 El Niño compared with those in the 1999 La Niña. Daily otolith increment widths, an estimator of somatic growth, corroborated population data. Between June 1 and August 9, mean increment widths for juvenile chinook salmon in 1998 were 3.54 ± 0.03 μm, significantly larger than the 3.13 ± 0.03 μm found in juveniles during the same time interval in 1999. Condition factor for juvenile chinook salmon entering the ocean at the Golden Gate was the same in both years, but became significantly greater in ocean fish during the 1998 El Niño than in ocean fish during the 1999 La Niña. Energy storage was significantly greater in ocean juvenile salmon during the 1998 El Niño as well. Mean triacylglycerol/cholesterol ratios increased following ocean entry in 1998, whereas they declined in ocean juveniles during 1999. Thus, not only was growth better in the El Niño period compared with La Niña, but lipid accumulation was also better. Oceanographic data for 1998 indicated elevated temperatures, lower salinity, greater freshwater outflow from San Francisco Bay, northerly flowing coastal currents, and positive upwelling index anomalies. This combination of environmental factors resulted in greater zooplankton productivity that, in conjunction with higher temperatures, allowed metabolic processes to enhance growth. Although El Niño events have certainly produced large‐scale, and often adverse, effects on ecosystems, the results of this study emphasize the importance of local oceanographic conditions to growth and other physiological and ecological processes.
Spatial correspondence between areas of concentration of Patagonian scallop (Zygochlamys patagonica) and frontal systems in the southwestern Atlantic
Authors: BOGAZZI EUGENIA , BALDONI ANA , RIVAS ANDRÉS , MARTOS PATRICIA , RETA RAÚL , ORENSANZ J. M. (LOBO) , LASTA MARIO , DELL'ARCIPRETE PATRICIA , WERNER FRANCISCO 
Published: September 2005

AbstractIt has been hypothesized that the geographical location of scallop beds in extensive shelf regions mirrors hydrographic structures (e.g. frontal systems) that favor the retention/concentration of pelagic larvae. Large, discontinuous concentrations of the Patagonian scallop (Zygochlamys patagonica) are known to have occurred recurrently (for more than 30 yr) at certain geographical locations over the extensive Patagonian shelf. These stocks, exploited since 1996, currently support one of the most important scallop fisheries in the world. Here, we investigate whether those aggregations are spatially coincidental with major frontal systems. Several pieces of information were used: historical survey data documenting the geographic distribution of the Patagonian scallop beds, catch and effort data from the commercial fleet, oceanographic data on frontal systems, and remote sensing imagery. We found that large‐scale aggregations do match the location of three major and very different frontal systems in the southwestern Atlantic: the Shelf‐Break Frontal System, the Northern Patagonia Frontal System, and the Southern Patagonia Frontal System. We describe the three frontal systems and their associated scallops fishing grounds and discuss which processes can contribute to sustaining the productivity of the scallop grounds in each case.