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Objective Anxiety is among the major psychological concerns for children living with food allergy (FA). Yet research exploring the variables driving anxiety symptoms in FA remains sparse, and most studies still utilize homogeneous samples to assess anxiety symptoms. The current study seeks to evaluate the rates of clinically significant anxiety symptoms among a diverse sample of youth with FA and examine whether a heightened risk perception of FA outcomes and FA burden (vs. FA medical history) is associated with anxiety in youth. Methods 94 youth ages 10–14 and their parents were recruited from FA clinics at a mid-Atlantic children's hospital. Both youth and parents completed demographic and FA medical history questionnaires, the Screen for Child Anxiety Related Emotional Disorders, and the Food Allergy Independent Measure as part of a longitudinal study about FA adjustment and adherence. Results Over a third (37%) of youth scored above clinical cut-offs for overall anxiety symptoms. At least 25% of youth reported clinically significant scores on panic disorder, generalized anxiety, social anxiety, separation anxiety, and school avoidance subscales. Perception of risk of adverse FA outcomes and burden—but not FA medical history–were associated with total anxiety, generalized anxiety, panic disorder, and school avoidance symptoms, but not social anxiety and separation anxiety. Having more FAs was associated with higher social anxiety scores but not with other anxiety subscales. Conclusions Youth with FA might benefit from psychosocial interventions that address FA risk perception management and promote appropriate FA vigilance to cope with anxiety symptoms. [ABSTRACT FROM AUTHOR]

Asthma, a prevalent chronic respiratory condition affecting millions of children globally, presents a significant health challenge. This review critically examines the developmental pathways of asthma in children, focusing on genetic, environmental, and early-life determinants. Specifically, we explore the impact of prenatal and postnatal factors such as maternal smoking, nutrition, respiratory infections, and allergen exposure on asthma development. Our analysis highlights the intricate interplay of these influences and their contribution to childhood asthma. Moreover, we emphasize targeted strategies and interventions to mitigate its burden, including genetic counseling for at-risk families, environmental modifications to reduce triggers, and early-life immunomodulation. By delving into these preventive measures and interventions, our review aims to provide actionable insights for healthcare professionals in developing tailored strategies to address the complexities of childhood asthma. In summary, this article offers a detailed examination of asthma development in children, aiming to enhance understanding and inform efforts to reduce its burden through targeted interventions. [ABSTRACT FROM AUTHOR]

Background: Allergic rhinitis (AR) is a typical type 2 inflammatory disease and eosinophils play a critical role of cardinal effectors in type 2 inflammation. However, the distribution of eosinophils in patients with different subtypes of rhinitis and the effect of allergen exposure on them remain understudied. The aim of this study was to investigate the characteristics and factors influencing the distribution of systemic and local eosinophils in patients with non-AR (NAR), perennial AR (PAR), and seasonal AR (SAR), as well as the effect of seasonal allergen exposure levels on eosinophils. Methods: This was a population-based, cross-sectional observational study of consecutive chronic rhinitis (CR) outpatients who volunteered to participate in the survey during the spring pollen season and non-pollen season of 2023 in Beijing. All participants underwent serum allergen testing, blood routine examination, and nasal secretion smear cytology, and completed questionnaires mainly involving basic information, history review, and symptom assessment. Spring pollen dispersal concentration were considered. Results: A total of 558 CR patients eligible for enrollment were collected, including 198 NAR, 204 PAR, and 156 SAR patients. PAR had the highest blood eosinophil levels and the most severe overall nasal and ocular symptoms of SAR. Compared with subjects with blood eosinophil counts

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BackgroundRegulatory T cells (Tregs) contribute to the maintenance of immunological tolerance. There is evidence of impaired function of these cells in people with asthma and allergy. In this study, we evaluated and compared the function of Tregs in allergic asthmatic and allergic non-asthmatic patients, both before and after low-dose allergen challenges.MethodsThree groups of subjects were recruited for a baseline evaluation: healthy controls without allergy or asthma, allergic asthmatic subjects, and allergic non-asthmatic subjects. All of them were subjected to expiratory flow measurements, sputum induction, and blood sampling. In addition, both groups of allergic subjects underwent low-dose allergen challenges. Tregs were isolated from whole blood using CD4+CD25high and CD127low staining. The suppression function was measured by flow cytometry. The levels of IL-10, IFN-γ, IgG4, IgA, and TGF-β were measured using ELISA, and sputum Foxp3 was evaluated using qRT-PCR.ResultsThe suppressive function of Tregs in healthy controls was significantly higher than in allergic asthmatic or allergic non-asthmatic subjects. Repeated exposure to low doses of allergen increased the suppressor function of Tregs in allergic non-asthmatic subjects but decreased it in allergic asthmatic subjects. Foxp3 gene expression was increased in induced sputum in allergic non-asthmatic subjects, whereas it did not change in asthmatic subjects. Serum IL-10 level was decreased in allergic asthmatic subjects after allergen challenge but not in allergic non-asthmatic subjects. IFN-γ level increased upon allergen challenge in allergic non-asthmatic subjects. IgG4 level was higher in allergic non-asthmatic subjects than in allergic asthmatic subjects.ConclusionsLow-dose allergen challenges stimulate the suppressor function of Tregs in non-asthmatic allergic subjects but not in allergic asthmatic subjects.

Abstract Background The typical clinical symptoms of allergic rhinitis (AR) are known to be associated with allergen exposure; however, the underlying mechanisms are not fully understood. We wanted to gain a comprehensive view of the molecular mechanisms related to allergen exposure in a well-controlled mouse model of AR. Methods An OVA-induced AR model was developed. Two hours and 4 weeks after the last OVA challenge, AR symptoms and local immune responses were assessed. At the same time, differentially expressed genes (DEG) in nasal mucosa were identified by gene expression microarray and further analyzed by bioinformatics methods. Verification of DEG was done by quantitative RT-PCR and immunohistochemistry. Results The number of nasal rubbings and sneezes, serum OVA-specific IgE concentrations, and the number of neutrophils and eosinophils in the nasal mucosa were significantly increased at 2 h and decreased at 4 weeks after the last allergen challenge compared to controls. A total of 2119 DEG were identified, and their expression dynamics were clustered into 8 profiles. Enriched functions in Profile 5, which had a similar trend to clinical features, were mainly related to inflammatory and immune response to environmental factors, eosinophils and neutrophils chemotaxis, and cell migration. Gene co-expression Network for genes from profile 5 identified BCL3, NFKB2, SOCS3, and CD53 having a higher degree. Profile 6 showed persistence of inflammatory and immune response at 4 weeks after the last allergen challenge. Olfactory and coagulation functions were enriched mainly in profiles with downward trends. Conclusions A wide range of genes with sequential cooperative action were identified to be associated with allergen exposure in AR. BCL3 may be the most vital in symptoms manifestation. Moreover, some inflammatory responses persisted for a period after allergen exposure, supporting a new treatment strategy of targeting inflammation out of season. This study may contribute to a better understanding of AR pathogenesis and provide potential therapeutic targets for AR patients.

Background: The typical clinical symptoms of allergic rhinitis (AR) are known to be associated with allergen exposure; however, the underlying mechanisms are not fully understood. We wanted to gain a comprehensive view of the molecular mechanisms related to allergen exposure in a well-controlled mouse model of AR. Methods: An OVA-induced AR model was developed. Two hours and 4 weeks after the last OVA challenge, AR symptoms and local immune responses were assessed. At the same time, differentially expressed genes (DEG) in nasal mucosa were identified by gene expression microarray and further analyzed by bioinformatics methods. Verification of DEG was done by quantitative RT-PCR and immunohistochemistry. Results: The number of nasal rubbings and sneezes, serum OVA-specific IgE concentrations, and the number of neutrophils and eosinophils in the nasal mucosa were significantly increased at 2 h and decreased at 4 weeks after the last allergen challenge compared to controls. A total of 2119 DEG were identified, and their expression dynamics were clustered into 8 profiles. Enriched functions in Profile 5, which had a similar trend to clinical features, were mainly related to inflammatory and immune response to environmental factors, eosinophils and neutrophils chemotaxis, and cell migration. Gene co-expression Network for genes from profile 5 identified BCL3, NFKB2, SOCS3, and CD53 having a higher degree. Profile 6 showed persistence of inflammatory and immune response at 4 weeks after the last allergen challenge. Olfactory and coagulation functions were enriched mainly in profiles with downward trends. Conclusions: A wide range of genes with sequential cooperative action were identified to be associated with allergen exposure in AR. BCL3 may be the most vital in symptoms manifestation. Moreover, some inflammatory responses persisted for a period after allergen exposure, supporting a new treatment strategy of targeting inflammation out of season. This study may contribute to a better understanding of AR pathogenesis and provide potential therapeutic targets for AR patients. [ABSTRACT FROM AUTHOR]

Severe asthma (SA) is categorized into multiple overlapping phenotypes and clinical characteristics driven by complex mechanistic inflammatory pathways. Mepolizumab is a human monoclonal antibody effectively targeting interleukin-5 in severe eosinophilic asthma. However, the eligibility of biologics in coincident SA phenotypes is still unclear. We assessed the efficacy and safety of mepolizumab in real-life patients with the overlapping T2-high SA endotype. This was a phase IV, single-centre observational cohort study including patients with severe refractory T2-high asthma in treatment with mepolizumab. After 12 months of treatment with mepolizumab, significant improvements (p < 0.0001) in asthma control and lung function were recorded. Rates of clinically significant annual asthma exacerbation were also decreased by 71.22% after 52-week therapy with mepolizumab (p < 0.001) associated with a reduction in the mean daily dose of oral corticosteroids. Two patients (3.27%) had to discontinue mepolizumab due to musculoskeletal disorders with no severe safety issues reported. The use of mepolizumab as an add-on therapy in routine clinical practice was safely associated with significant clinical and functional in the overlapping eosinophilic-and-allergic SA phenotype. The current data should support clinical and therapeutic decision-making in this T2-high SA endotype. [ABSTRACT FROM AUTHOR]

The links between allergen exposure and sensitization are complex and depend not only on the type of allergen but on various genetic and environmental factors. This review discusses the link between allergen exposure and atopic sensitization for different types of allergens and the factors that mediate or affect this link. For the purposes of this review search of PubMed was undertaken to identify English language articles using the terms 'sensitization' and 'allergen exposure' and 'children/or adolescents.' Regarding food sensitization, the available data for peanuts and eggs suggest that there is a window period between 4 and 6 months of age when the introduction of these foods may limit sensitization and clinically overt allergy to the respective foods. As far as it concerns aeroallergens, it seems that there is a complex and variable relationship between mite exposure and specific sensitization especially if the exposure occurs early in life. Early exposure to dog allergens does not seem to be associated with specific sensitization; regarding cats, the results are still inconsistent. Several factors may mediate the relationship between early exposure to allergens and the development of sensitization or clinical allergy. [ABSTRACT FROM AUTHOR]

Storage mites (SM) may induce allergic respiratory symptoms in sensitized individuals, in both rural and urban settings. The relationship among specific IgE reactions to determined groups of SM allergens in the coincident asthma pheno-endotypes has not yet been investigated. We aimed to study a Precision Allergy Molecular Diagnosis (PAMD@) model to depict the SM molecular profile in individuals presenting with Type-2 inflammation, in two different (moderate and severe) asthma phenotypes. A customized PAMD@ panel, including SM allergens and their concurrent protein allergenic characterization was investigated. Mite group 2 allergens were most frequently recognized, including Lep d 2 (83.45%), followed by Gly d 2 (69.17%) and Tyr p 2 (47,37%), in 133/164 asthmatic subjects. Blo t 5 and Blo t 21 exhibited significant higher titres in both asthma groups. Although relevant mite group 2 allergens cross-reactivity is suggested, individualized sensitization patterns were relevantly identified. The present PAMD@ panel confirmed the dominance of mite group 2 allergens in moderate-to-severe T2 asthmatics. A broadly heterogeneous molecular repertoire of SM allergens was found in all subjects, regardless of their asthma severity. Blomia tropicalis deserves special attention in certain territories, as diagnostic and/or therapeutic approaches merely based on Pyroglyphidae mites may be insufficient. [ABSTRACT FROM AUTHOR]

BackgroundProtease resistance is considered a risk factor for allergenicity of proteins, although the correlation is low. It is nonetheless a part of the weight-of-evidence approach, proposed by Codex, for assessing the allergenicity risk of novel food proteins. Susceptibility of proteins to pepsin is commonly tested with purified protein in solution.ObjectiveFood proteins are rarely consumed in purified form. Our aim was to evaluate the impact of experimental and endogenous food matrices on protease susceptibility of homologous protein pairs with different degrees of allergenicity.MethodsPorcine and shrimp tropomyosin (ST) were subjected to sequential exposure to amylase, pepsin, and pancreatin in their respective endogenous matrix (pork tenderloin/boiled shrimp) and in three different experimental matrices (dessert mousse [DM], soy milk [SM], and chocolate bar [CB]). Digestion was monitored by immunoblotting using tropomyosin-specific antibodies. Recombinant peach and strawberry lipid transfer protein were biotinylated, spiked into both peach and strawberry fruit pulp, and subjected to the same sequential digestion protocol. Digestion was monitored by immunoblotting using streptavidin for detection.ResultsChocolate bar, and to a lesser extent SM, had a clear protective effect against pepsin digestion of porcine tropomyosin (PT) and to a lesser extent of ST. Increased resistance was associated with increased protein content. Spiking experiments with bovine serum albumin (BSA) confirmed the protective effect of a protein-rich matrix. The two tropomyosins were both highly resistant to pepsin in their protein-rich and lean native food matrix. Pancreatin digestion remained rapid and complete, independent of the matrix. The fat-rich environment did not transfer protection against pepsin digestion. Spiking of recombinant peach and strawberry lipid transfer proteins into peach and strawberry pulp did not reveal any differential protective effect that could explain differences in allergenicity of both fruits.ConclusionsProtein-rich food matrices delay pepsin digestion by saturating the protease. This effect is most apparent for proteins that are highly pepsin susceptible in solution. The inclusion of food matrices does not help in understanding why some proteins are strong primary sensitizers while homologs are very poor allergens. Although for induction of symptoms in food allergic patients (elicitation), a protein-rich food matrix that may contribute to increased risk, our results indicate that the inclusion of food matrices in the weight-of-evidence approach for estimating the potential risks of novel proteins to become allergens (sensitization), is most likely of very limited value.

Rationale: Environmental exposures have been associated with adverse outcomes in chronic obstructive pulmonary disease (COPD). Approximately one-third of individuals with COPD have allergic sensitization, but it is unknown whether exposure to allergens in the home is associated with outcomes. Objectives: To determine the prevalence and associations of allergen sensitization with exposure to common indoor allergens with symptoms and exacerbation risk in COPD. Methods: Allergen sensitization to five common indoor allergens was assessed in former smokers with COPD. Home settled dust was assessed for presence of corresponding allergens. Sensitization and exposure status was determined and associations evaluated in adjusted models with longitudinal outcomes including symptoms, lung function, and exacerbations. Interactions were assessed between sensitization/exposure status and lung function. Measurements and Main Results: One hundred eighty-three individuals studied were on average 67.3 years of age (SD, 8.22) with average FEV1 of 53.2% (SD, 17.6%). Seventy-seven percent of participants were exposed to at least one tested allergen, and 17% had sensitization with corresponding allergen exposure. After adjustment, sensitization with exposure was associated with lower lung function (β, -8.29; 95% confidence interval [CI], -14.80 to -1.77), higher St. George's Respiratory Questionnaire Total Score (β, 6.71; 95% CI, 0.17 to 13.25), and higher exacerbation risk (odds ratio, 2.31; 95% CI, 1.11 to 4.79). Associations appeared to be more pronounced among individuals with lower lung function. Conclusions: Allergen exposures are common in COPD and associated with adverse outcomes among those with concomitant allergen sensitization. This study establishes allergens as an important home exposure that potentially could be addressed with comprehensive home environmental modification strategies to improve COPD outcomes. [ABSTRACT FROM AUTHOR]

Severe asthma (SA) is categorized into multiple overlapping phenotypes and clinical characteristics driven by complex mechanistic inflammatory pathways. Mepolizumab is a human monoclonal antibody effectively targeting interleukin-5 in severe eosinophilic asthma. However, the eligibility of biologics in coincident SA phenotypes is still unclear. We assessed the efficacy and safety of mepolizumab in real-life patients with the overlapping T2-high SA endotype. This was a phase IV, single-centre observational cohort study including patients with severe refractory T2-high asthma in treatment with mepolizumab. After 12 months of treatment with mepolizumab, significant improvements (p < 0.0001) in asthma control and lung function were recorded. Rates of clinically significant annual asthma exacerbation were also decreased by 71.22% after 52-week therapy with mepolizumab (p < 0.001) associated with a reduction in the mean daily dose of oral corticosteroids. Two patients (3.27%) had to discontinue mepolizumab due to musculoskeletal disorders with no severe safety issues reported. The use of mepolizumab as an add-on therapy in routine clinical practice was safely associated with significant clinical and functional in the overlapping eosinophilic-and-allergic SA phenotype. The current data should support clinical and therapeutic decision-making in this T2-high SA endotype.

Background: Sensitization to house dust mite (HDM) is a leading cause of allergic rhinitis and asthma. Despite more than 30 HDM‐derived allergens having been identified to date, specific therapeutic approaches do not yet take into account the local sensitization profiles of patients. This study aimed to identify patterns of HDM sensitization in HDM‐allergic adults living in distinct geographic areas, to inform the development of targeted diagnostic and therapeutic tools. Methods: Serum samples from 685 HDM‐allergic subjects from Canada, Europe, South Africa, and the USA were tested for levels of IgE specific for 17 micro‐arrayed HDM allergens by ImmunoCAP Immuno Solid‐phase Allergen Chip (ISAC) technology. Results: The results confirmed significant geographical variability in sensitization patterns and levels of IgE. In all areas, the major sensitizers were the group 1 and group 2 allergens and Der p 23. Der p 23 was a frequent sensitizer: 64% of the subjects had IgE specific for Der p 23, and 2.3% were monosensitized to it. In South Africa, Der p 23 was the dominant HDM allergen (86% prevalence) and Der p 7 achieved major allergen status (56%). IgE sensitization to HDM was influenced by asthmatic status, levels of allergen exposure, age, race‐ethnicity and smoking status, but not by BMI. Conclusion: Sensitization profiles to HDM allergens differ considerably among distinct geographic areas, with Der p 7 and Der p 23 being major sensitizers in South Africa. Such heterogeneity should be taken into account in the diagnosis and treatment of HDM‐allergic patients. [ABSTRACT FROM AUTHOR]

Background: The association among the IgE responses to prevailing groups of house dust mite (HDM) allergens in the concurrent asthma phenotypes has not been determined. Objective: The aim of the present study lays on a component-resolved diagnosis (CRD) model to investigate the mite molecular signature in subjects with type-2 inflammation asthma. Methods: We selected patients showing a clinically relevant sensitization to HDMs with moderate-to-severe persistent asthma. Skin prick test (SPT) with standardized mite extracts, a broad customized CRD serum sIgE panel including 9 Dermatophagoides pteronyssinus allergens and the related protein allergenic characterization, was investigated in all serum samples. Results: Ninety out of 93 (96.77%) patients with a positive SPT to HDM showed a concordant sIgE (≥0.35 kUA/L) to the crude extract of D. pteronyssinus. Major allergens (Der p 2, Der p 23, and Der p 1) were present in >70% of all subjects, with mid-tier allergens (Der p 5, Der p 7, and Der p 21) reaching up to 51% in the present cohort. A complex pleomorphic repertoire of HDM molecules recognized by IgE was depicted, including 38 distinct profiles. Conclusions and Clinical Relevance: The proposed CRD panel approach, containing the most prevalent HDM allergens, appeared to be sufficient to obtain a precise D. pteronyssinus molecular diagnosis in asthmatics with a climate-dependent high-mite allergen exposure and coexisting sensitization. A dominant role of both major and mid-tier allergens has been confirmed in moderate and severe persistent asthmatics with the preponderant Th2-high endotype. [ABSTRACT FROM AUTHOR]

Background: In pollinosis patients, allergen-specific antibody titers show seasonal variations. Little is known about these variations at the epitope level. Objectives: We aimed at investigating seasonal variations on the level of allergen epitope recognition in patients with Bet v 1-related food allergy using a peptide phage display approach. Methods: Serum samples collected over 1 year from 4 patients of the placebo arm of the birch-associated soya allergy immunotherapy trial were included. To identify epitopes from Bet v 1-related food allergens, patient sera were used in peptide phage display experiments. In silico analysis of enriched allergen-related motifs was performed. Results: We identified epitope motifs related to Bet v 1 and its homologs in soya and hazelnut (Gly m 4 and Cor a 1, respectively) that were enriched in accordance with birch and hazel pollen exposure. Within several weeks after the birch pollen season peak, the pattern of identified epitope motifs differed considerably among patients. Data for amino acid preferences in homologous Bet v 1 and Cor a 1 epitope motifs identified for one of the investigated patients suggest changes in concentration or specificity of serum antibodies for the Cor a 1 epitope motif. Conclusions: Peptide phage display data suggest an impact of birch and hazel pollen exposure on the recognition pattern of Bet v 1-like allergen epitopes. Epitope-oriented analyses could provide deeper, personalized details regarding the allergen epitope recognition influenced by pollen exposure beyond the capability of current methods. [ABSTRACT FROM AUTHOR]

We hypothesized that filaggrin (FLG) loss-of-function mutations modify the effect of allergen exposure on the development of allergic sensitization. We sought to determine whether early-life exposure to inhalant allergens increases the risk of specific sensitization and whether FLG mutations modulate these odds. In a population-based birth cohort we measured mite, cat, and dog allergen levels in dust samples collected from homes within the first year of life. Sensitization was assessed at 6 time points between infancy and age 16 years. Genotyping was performed for 6 FLG mutations. In the longitudinal multivariable model (age 1-16 years), we observed a significant interaction between FLG and Fel d 1 exposure on cat sensitization, with the effect of exposure being significantly greater among children with FLG mutations compared with those without (odds ratio, 1.36; 95% CI, 1.02-1.80; P =.035). The increase in risk of mite sensitization with increasing Der p 1 exposure was consistently greater among children with FLG mutations, but the interaction did not reach statistical significance. Different associations were observed for dogs: there was a significant interaction between FLG and dog ownership, but the risk of sensitization to any allergen was significantly lower among children with FLG mutations who were exposed to a dog in infancy (odds ratio, 0.16; 95% CI, 0.03-0.86; P =.03). FLG loss-of-function mutations modify the relationship between allergen exposure and sensitization, but effects differ at different ages and between different allergens. [ABSTRACT FROM AUTHOR]

Summary: Although acute prophylactic administration of atropine modulates airway responsiveness, the role of the parasympathetic nervous system in the pathogenesis of sensitization and in antigen‐induced bronchoconstriction remains unclear. The aim of the present study is to determine whether blocking muscarinic receptors during chronic allergen exposure modulates lung responsiveness to the specific allergen. Forty rats were randomly assigned to one of the following five treatment groups: sensitization with saline vehicle, intraperitoneal injection of ovalbumin (1 mg) with or without atropine treatment (10 mg/kg per day) and repeated ovalbumin aerosol (1.25 mg/mL for 20 minutes) either alone or combined with atropine. Lung responsiveness to methacholine (4–16 μg/kg per minute) and intravenous ovalbumin (2 mg) was established before and 21 days after treatment with forced oscillations following bilateral vagotomy. Lung cellularity was determined by analysis of bronchoalveolar lavage fluid (BALF). A lung inflammatory response in all sensitized animals was defined as an increase in the number of inflammatory cells in the BALF. Baseline respiratory mechanics and methacholine responsiveness on Days 0 and 21 were comparable in all groups. However, increases in airway resistance following intravenous allergen challenge were significantly exacerbated in rats that received atropine. Inhibition of the cholinergic nervous system during allergic sensitization potentiates bronchoconstriction following exposure to the specific allergen. These findings highlight the role of the cholinergic neuronal pathway in airway sensitization to a specific allergen. [ABSTRACT FROM AUTHOR]

Background: Details of the current UK drug and allergen exposure were needed for interpretation of reports of perioperative anaphylaxis to the 6th National Audit Project (NAP6).Methods: We performed a cross-sectional survey of 356 NHS hospitals determining anaesthetic drug usage in October 2016. All cases cared for by an anaesthetist were included.Results: Responses were received from 342 (96%) hospitals. Within-hospital return rates were 96%. We collected 15 942 forms, equating to an annual caseload of 3.1 million, including 2.4 million general anaesthetics. Propofol was used in 74% of all cases and 90% of general anaesthetics. Maintenance included a volatile agent in 95% and propofol in 8.7%. Neuromuscular blocking agents were used in 47% of general anaesthetics. Analgesics were used in 88% of cases: opioids, 82%; paracetamol, 56%; and non-steroidal anti-inflammatory drugs, 28%. Antibiotics were administered in 57% of cases, including 2.5 million annual perioperative administrations; gentamicin, co-amoxiclav, and cefuroxime were most commonly used. Local anaesthetics were used in 74% cases and 70% of general anaesthetics. Anti-emetics were used in 73% of cases: during general anaesthesia, ondansetron in 78% and dexamethasone in 60%. Blood products were used in ≈3% of cases, gelatin <2%, starch very rarely, and tranexamic acid in ≈6%. Chlorhexidine and povidone-iodine exposures were 74% and 40% of cases, and 21% reported a latex-free environment. Exposures to bone cement, blue dyes, and radiographic contrast dye were each reported in 2-3% of cases.Conclusions: This survey provides insights into allergen exposures in perioperative care, which is important as denominator data for the NAP6 registry. [ABSTRACT FROM AUTHOR]

Abstract: Background: Early‐life sensitization to indoor allergens predicts asthma development. The aim of this study was to compare allergen concentrations in day‐care centers (DCC) with those in private homes. Methods: Settled airborne dust was collected 4 times a year from 20 German DCC (620 samples) and from the homes of children and day‐care workers (602 samples) using electrostatic dust collectors (EDC). The samples were analyzed with fluorescence enzyme immunoassays recognizing domestic mite allergens (DM), Fel d 1, Can f 1, and Mus m 1. Pet allergen thresholds that discriminate samples from homes with cats or dogs from those without were calculated using receiver‐operating characteristics. Influences on allergen levels were analyzed using multilevel models. Results: Allergen loads were on average higher in DCC than in homes. In DCC, 96% of the samples were positive for DM, 95% for Can f 1, 90% for Fel d 1, and 83% for Mus m 1. In homes, 84% contained DM, 48.5% Can f 1, 33% Fel d 1, and 43% Mus m 1. The threshold level for homes with dogs was 75 ng/m² Can f 1 (96.8% sensitivity, 96% specificity), and the threshold level for homes with cats was 46 ng/m² Fel d 1 (92% sensitivity, 94.9% specificity). In DCC, Can f 1 and Fel d 1 loads were higher than these thresholds in 37% and 54% of the samples, respectively. Allergen levels were significantly influenced by the season and room type; however, carpets on floors had no influence. Conclusions: Mite, mouse, cat, and dog allergens were mostly higher in DCC than in homes. Exposure to dog and cat allergens in DCC often reached levels of households with pets. [ABSTRACT FROM AUTHOR]

Ovalbumin (OVA) sensitization has limitations in modelling asthma. Thus, we examined the value of allergic sensitization using a purified natural allergen, house dust mite (HDM), over the sensitization performed with OVA. Mice were sham-treated, or sensitized with OVA- or HDM with identical chronology. Airway resistance, tissue damping and elastance were assessed under control conditions and after challenging the animals with methacholine (MCh) and the specific allergen. Inflammatory profile of the bronchoalveolar lavage fluid was characterized and lung histology was performed. While no difference in the lung responsiveness to the specific allergen was noted, hyperresponsiveness to MCh was observed only in the HDM-sensitized animals in the lung peripheral parameters. Lung inflammation differed between the models, but excessive bronchial smooth muscle remodelling occurred only with OVA. In conclusion, we demonstrate that a purified natural allergen offers a more relevant murine model of human allergic asthma by expressing the key features of this chronic inflammatory disease both in the lung function and structure. [ABSTRACT FROM AUTHOR]

[i]Chaetomium globosum [/i]is one of the most common fungi that grows in damp buildings and occurs in agricultural and forestry workplaces. Using sera from atopic patients, we characterized and purified an extracellular chitosanase (Chg47) from [i]C. globosum[/i] that is antigenic to humans. The study reports the production of monoclonal antibodies to the protein. Three capture ELISAs were developed for Chg47 for detection of spores and spore and mycelial fragments in dust samples using different mono- and polyclonal antibody combinations. One method is based on an enhanced biotinylated polyclonal antibody as the secondary antibody and coating anti-IgM to capture one of two clones of IgM monoclonal antibodies as the capture antibody. The other method makes use of an enhanced rabbit polyclonal antibody as both the primary and capture antibody. The detection limit of the double PAb method for the Chg47 antigen was 7.6 pg/ml. When the anti-IgM+10B3 clone was used, the detection limit was 61 pg/ml and for anti-IgM+5F12, 122 pg/ml. The detection limit of double PAb method is comparable to methods for the allergen and spores of [i]Aspergillus versicolor[/i] in house dust and is more sensitive than other immunoassays for allergens in house including for [i]Stachybotrys chartarum[/i], [i]Aspergillus fumigatus[/i] and [i]Alternaria alternata[/i]. All three methods had limited cross-reactivity to fungi common in house dust representing a diverse array of taxa.

This review aims to present in a simple manner the work performed in Portugal regarding the identification of the most prevalent aeroallergens in the country and the sensitization levels in Portuguese patients. Much of the data was summarized in tables and illustrated on maps, enabling the community of clinicians, researchers, and patient organizations to access the knowledge about the research performed. This study provides an overview about the distribution of aeroallergens in Portugal, signaling regions and critical periods of exposure of the sensitized population. The illustrated data can help the community of allergy specialists to view the temporal and spatial distribution of aeroallergens across the country. In addition, this information can guide clinicians to select the most appropriate allergens for allergy diagnostic testing, treatment, and allergen avoidance. [ABSTRACT FROM AUTHOR]

Allergic rhinitis (AR) has been a significant healthcare burden on individuals and society. However, the detailed effect of different patterns of allergen exposure on the development of AR remains controversial. A mouse model of AR was established to address the complex relationships between allergen exposure and the development of AR. Allergic symptom, OVA-specific IgE in serum and nasal lavage fluid, allergic inflammation in nasal tissues were evaluated after intranasal sensitization and challenge of ovalbumin (OVA) in mice treated with two different doses of allergen for different sensitized durations. Exposure to different doses and sensitized durations of OVA were capable of inducing allergic nasal response. Repetitive OVA exposure in the sensitization phase induced the recruitment of eosinophils and goblet cell hyperplasia. The level of OVA-specific IgE in serum depended on OVA exposure and was mediated in a duration-related manner. In addition, mice treated with low-dose OVA for prolonged duration manifested the major features of human local allergic rhinitis. There were dose- and duration-related effects of allergen exposure on the development of AR. LAR was associated with repetitive exposure to low-dose allergen. Thus, allergen avoidance should be an important aim of AR management. [ABSTRACT FROM AUTHOR]

Background The relation between IgE sensitization and allergic respiratory symptoms has usually been evaluated by dichotomizing specific IgE levels. The aim of this study was to evaluate the association between specific IgE levels and risk of symptoms on allergen-related exposure, with special reference to allergen-related asthma-rhinitis comorbidity. Methods We considered 6391 subjects enrolled within the European Community Respiratory Health Survey 2, having information on cat/grass/ D. pteronyssinus IgE levels and symptoms on exposure to animals/pollen/dust. The risk of oculonasal/asthmalike/both symptoms was evaluated by a multinomial logistic model. Results A clear positive association was observed between specific IgE levels to cat/grass/mite and the risk of symptoms on each allergen-related exposure (test for trend with P < 0.001). This trend was particularly pronounced when considering the coexistence of asthmalike and oculonasal symptoms. Compared to non-sensitized subjects, subjects with specific IgE to cat >= 3.5 kU/l presented relative risk ratios of 11.4 (95% CI 6.7-19.2), 18.8 (8.2-42.8), and 55.3 (30.5-100.2) when considering, respectively, only oculonasal symptoms, only asthmalike symptoms, or both. A similar pattern was observed when considering specific IgE to grass/mite and symptoms on exposure to pollen/dust. Also the proportion of people using inhaled medicines or visiting a general practitioner for breathing problems in the previous year increased with increasing sum of specific IgE to cat/grass/mite. Conclusion Specific IgE level is the most important predictor of allergen-related symptoms. The risk of both oculonasal/asthmalike symptoms increases with specific IgE levels, suggesting that specific IgE contributes to the 'united airways disease'. [ABSTRACT FROM AUTHOR]

Furry mammals kept as pets, farm and laboratory animals are important allergen sources. The prevalence of sensitization to furred mammals appears to be increasing worldwide. Several mammalian allergens from diverse species are well characterized with regard to their molecular structure and immunogenicity, and some are already available for component-resolved allergy diagnostics. The distribution of various mammalian allergens has been extensively studied during the past few decades. Animal allergens were found to be ubiquitous in the human environment, even in places where no animals reside, with concentrations differing considerably between locations and geographical regions. This review presents an overview of identified mammalian respiratory allergens classified according to protein families, and compiles the results of allergen exposure assessment studies conducted in different public and occupational environments.

It is estimated that pollen allergies affect approximately 40% of allergic individuals. In general, tree pollen allergies are mainly elicited by allergenic trees belonging to the orders Fagales, Lamiales, Proteales, and Pinales. Over 25 years ago, the gene encoding the major birch pollen allergen Bet v 1 was the first such gene to be cloned and its product characterized. Since that time, 53 tree pollen allergens have been identified and acknowledged by the WHO/ IUIS allergen nomenclature subcommittee. Molecule-based profiling of allergic sensitization has helped to elucidate the immunological connections of allergen cross-reactivity, whereas advances in biochemistry have revealed structural and functional aspects of allergenic proteins. In this review, we provide a comprehensive overview of the present knowledge of the molecular aspects of tree pollen allergens. We analyze the geographic distribution of allergenic trees, discuss factors pivotal for allergic sensitization, and describe the role of tree pollen panallergens. Novel allergenic tree species as well as tree pollen allergens are continually being identified, making research in this field highly competitive and instrumental for clinical applications. [ABSTRACT FROM AUTHOR]

Allergic diseases are a major cause of morbidity in the developed world, now affecting up to 40 % of the population with no evidence that this is abating. If anything, the prevalence of early onset allergic diseases such as eczema and food allergy appears to be still increasing. This is almost certainly due to the changing modern environment and lifestyle factors, acting to promote immune dysfunction through early perturbations in immune maturation, immune tolerance and regulation. This early propensity to inflammation may also have implications for the rising risk of other inflammatory non-communicable diseases (NCDs) later in life. Identifying risk factors and pathways for preventing early onset immune disease like allergy is likely to have benefits for many aspects of human health, particularly as many NCDs share similar risk factors. This review focuses on recent advances in primary intervention strategies for promoting early immune health and preventing allergic disease, highlighting the current evidence-based guidelines where applicable and areas requiring further investigation. [ABSTRACT FROM AUTHOR]

In cases of occupational asthma due to reactive chemicals, an appreciable number of patients have persistent asthmatic symptoms and airway inflammation even after several years' avoidance of the cause agents. A case of late respiratory systemic syndrome (LRSS) caused by phthalic anhydride is reported. The patient showed a progression of bronchial asthma due to house dust mite and developed a new bronchial sensitization to horse hair during the 5 year follow-up period. The patient was diagnosed in September 1990 as having LRSS due to phthalic anhydride. He was atopic and had worked in a factory preparing materials for paints for 8 years. After leaving his workplace and commencing treatment with anti-asthmatic medications, his asthmatic symptoms and airway hyper-responsiveness were much improved for 1year (PC20 methacholine level was increased from 0.44 to 4.4 mg/mL). For several months before the second admission (October 1992) his asthmatic symptoms were again aggravated and methacholine PC20 decreased to 1.1mg/mL without improvement in the following 3 years. The level of serum specific IgE antibody to phthalic anhydride has been gradually decreasing, while specific IgE to two types of house dust mite and horse hair has been increasing year by year during the last 3 years' follow-up period. These findings suggest that chronic exposure to inhalant allergens can induce the progression of allergen-induced airway inflammation, and result in new bronchial sensitization to inhalant allergens. Careful follow-up study is needed to detect new developments of allergen-induced bronchoconstriction in occupational asthma patients with persistent asthmatic symptoms.

Chaetomium globosum is one of the most common fungi that grows in damp buildings and occurs in agricultural and forestry workplaces. Using sera from atopic patients, we characterized and purified an extracellular chitosanase (Chg47) from C. globosum that is antigenic to humans. The study reports the production of monoclonal antibodies to the protein Three capture ELISAs were developed for Chg47 for detection of spores and spore and mycelial fragments in dust samples using different mono- and polyclonal antibody combinations. One method is based on an enhanced biotinylated polyclonal antibody as the secondary antibody and coating anti-IgM to capture one of two clones of IgM monoclonal antibodies as the capture antibody. The other method makes use of an enhanced rabbit polyclonal antibody as both the primary and capture antibody. The detection limit of the double PAb method for the Chg47 antigen was 7.6 pg/ml When the anti-lgM+10B3 clone was used, the detection limit was 61 pg/ml and for anti-lgM+5F12, 122 pg/ml. The detection limit of double PAb method is comparable to methods for the allergen and spores of Aspergillus versicolor in house dust and is more sensitive than other immunoassays for allergens in house including for Stachybotrys chartarum, Aspergillus fumigatus and Alternaria alternate.. All three methods had limited cross-reactivity to fungi common in house dust representing a diverse array of taxa. [ABSTRACT FROM AUTHOR]

Studies that estimate indoor aeroallergen exposure typically measure a pre-selected limited range of allergens. In this study, inhalable aeroallergen particles were quantified using the halogen immunoassay ( HIA) to determine the contribution of fungal and non-fungal aeroallergens to total allergen exposure. Bioaerosols from 39 homes of fungal-allergic subjects were sampled using inhalable fraction samplers and immunostained by HIA using resident subject's immunoglobulin E (IgE) to detect allergen-laden particles. Fungal aerosols as well as particles carrying mite, cat, and cockroach allergens were identified and enumerated by HIA. Reservoir dust-mite (Der p 1), cat (Fel d 1), and cockroach (Bla g 1) allergen concentrations were quantified by ELISA. Fungal particles that bound subject's IgE in the HIA were 1.7 (bedroom)- and 1.4 (living room)-fold more concentrated than Der p 1, Fel d 1, and Bla g 1 allergen particles combined. Predominant fungal conidia that bound IgE were derived from common environmental genera including Cladosporium and other fungi that produce amerospores. Airborne mite, cat, and cockroach allergen particle counts were not associated with reservoir concentrations determined by ELISA. This study demonstrates that inhalable fungal aerosols are the predominant aeroallergen sources in Sydney homes and should be considered in future exposure assessments. [ABSTRACT FROM AUTHOR]

Questions and commentary on the article ‘Daily changes of peak expiratory flow and respiratory symptom occurrence around a soy processing factory’

Bed bugs may cause mild to severe cutaneous reactions. We studied the ability of bed bug salivary extract (SGE) to induce inflammatory reactions responsible for cutaneous manifestations and found that SGE stimulated the production of several potent chemokines and cytokines from macrophages. Chemokines induced by SGE included those known to recruit eosinophils (eotaxin), attract neutrophils [interleukin (IL)-8] or induce their survival and proliferation (granulocyte colony-stimulating factor). Cytokines involved in cell-mediated immunity, including IL-7, IL-10 and IL-12, were also induced. Saliva of bed bugs contains protein and non-protein molecules that have pleotropic effects on macrophages, orchestrating the immune response in the skin after bed bug bites. Copyright © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Abstract: This nested case-control study examined the association between prevalent asthma and indoor allergen sensitization and/or exposure among children (aged 5–17 years) in Buffalo, New York. The study included a self-administered questionnaire, clinical interviews, skin allergen sensitivity tests and home dust sampling for house dust mites, cat, dog, cockroach and mouse allergens. After adjusting for multiple confounders, asthma cases had higher odds of being sensitized to Der p dust mites (odds ratio [OR]=1.94, 95% confidence interval (CI): 1.13–3.35), cat (OR=1.96, 95% CI: 1.13–3.39), or dog allergens (OR=1.89, 95% CI: 1.10–3.22) than the controls. A significantly positive association between asthma status presence of cat allergen in the child''s mattress (ORs: 2.61, 95% CI: 1.09–6.28) was also found. Children with both sensitization and environmental exposure to cat allergens had higher odds of asthma (OR=7.08, 95% CI: 2.12–23.62) than those who were only sensitized to cat allergen (OR=2.31, 95% CI: 1.01–5.32) or had only home exposures (OR=1.47, 95% CI: 0.47–4.65). The association between allergen sensitization and asthma was more consistent than for home exposures. The findings help to confirm the role of allergen sensitization and home exposure in regard to asthma, and suggest that both, individually and jointly, are associated with asthma. [Copyright &y& Elsevier]

Abstract: Insect bite hypersensitivity (IBH), an allergic reaction to the saliva of Culicoides, occurs in all horse breeds and is a severe problem. In this study, we aimed at exploring whether exterior conditions, such as duration of allergenic exposure during the first summer and age of the horses at the time of import, influence the development of IBH. Additionally, data were analyzed regarding the period IBH started after birth and after import. Datasets for 582 horses were collected. The horses were locally born Icelandic horses and horses of other breeds with IBH, as well as imported Icelandic horses, both affected and nonaffected. For locally born horses, time of birth and duration of allergen exposure during the first summer had no influence on the prevalence of IBH. The disease started mostly in their third year of life. The majority of the imported horses affected caught IBH during their first year in Central Europe. Older imported horses seemed to develop IBH quicker than younger animals. Animals imported in their first winter are exposed to the allergen when they are at least 7 months old. They experienced approximately the same low risk of developing IBH as locally bred horses. The risk of IBH increased with the horses’ age at import. From our data, we conclude that the period to develop successful immune tolerance goes beyond the perinatal phase and is longer than formerly supposed. [Copyright &y& Elsevier]

Background: In asthmatics, a rapid decline in pulmonary function is observed, likely as a consequence of airways remodeling. Persistence of allergen exposure in patients with occupational asthma (OA) maintains chronic bronchial inflammation, resulting in a more severe lung function decline. Few studies were performed on the effects of allergen exposure cessation. Objective: This study aims at evaluating the influence of allergen exposure cessation on respiratory decline in allergic asthmatic workers. Methods: Two groups of workers with allergic OA were selected. The first group (30 workers) changed job after the diagnosis and was no more exposed to sensitizing allergens, and the second group (28 subjects) did not and, as a consequence of preventive measures in the work place, was exposed to a lower level of allergens. All were treated with conventional therapy, according to GINA protocols. FEV1 changes during a 12-year period were evaluated. Results: Despite pharmacological therapy, the pulmonary function decay slope was steeper in workers continuously exposed to the sensitizing agent (even at reduced level) than in those with a complete cessation of exposure: final FEV1 loss was 512.5 ± 180 ml versus 332.5 ± 108 ml, respectively. The difference became significant after 4 years from the cessation of the exposure. Conclusions: The study shows that the cessation of the exposure to allergen in the work place appears the most effective measure in limiting pulmonary function decline in asthmatic workers and underlines the importance of allergic risk assessment and control in the management of occupational asthma. [ABSTRACT FROM AUTHOR]

Background: Seasonal allergic rhinitis (SAR) to Japanese cedar (Cryptomeria japonica; JC) is an IgE-mediated type I allergy affecting the nasal mucosa. However, the molecular mechanisms that underlie SAR are only partially understood. The aim of the study was to identify novel genes related to SAR during natural exposure to pollens, by using microarray analysis. Methods: Subjects were 32 SAR patients and 25 controls. Total RNA was extracted from CD4+ T cells isolated from peripheral blood mononuclear cells and subjected to microarray analysis with Illumina Human Ref8 BeadChip arrays. The Mann-Whitney test was performed to identify genes whose expression was altered during allergen exposure. Quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) was performed on samples collected from SAR patients and controls to verify the microarray results. Results: Microarray analysis showed that the expression of 3 genes was significantly altered during allergen exposure. Among these 3 genes, the expression of interleukin 17 receptor beta (IL17RB) was confirmed to be upregulated in SAR patients compared to that of the IL17RB gene in healthy, non-allergic controls. The average fold change of IL17RB expression in the real-time RT-PCR experiment was 3.9 (P = 0.003). Conclusions: The present study identified upregulation of IL17RB during natural allergen exposure in patients with SAR, which may further elucidate the molecular mechanisms underlying SAR. [ABSTRACT FROM AUTHOR]

To cite this article: Matsui EC, Sampson HA, Bahnson HT, Gruchalla RS, Pongracic JA, Teach SJ, Gergen PJ, Bloomberg GR, Chmiel JF, Liu AH, Kattan M, Sorkness CA, Steinbach SF, Story RE, Visness CM, on behalf of the Inner-city Asthma Consortium. Allergen-specific IgE as a biomarker of exposure plus sensitization in inner-city adolescents with asthma. Allergy 2010; 65: 1414-1422. Background: Relationships among allergen-specific IgE levels, allergen exposure and asthma severity are poorly understood since sensitization has previously been evaluated as a dichotomous, rather than continuous characteristic. Methods: Five hundred and forty-six inner-city adolescents enrolled in the Asthma Control Evaluation study underwent exhaled nitric oxide (FENO) measurement, lung function testing, and completion of a questionnaire. Allergen-specific IgE levels and blood eosinophils were quantified. Dust samples were collected from the participants' bedrooms for quantification of allergen concentrations. Participants were followed for 12 months and clinical outcomes were tracked. Results: Among sensitized participants, allergen-specific IgE levels were correlated with the corresponding settled dust allergen levels for cockroach, dust mite, and mouse ( r = 0.38, 0.34, 0.19, respectively; P < 0.0001 for cockroach and dust mite and P = 0.03 for mouse), but not cat ( r = −0.02, P = 0.71). Higher cockroach-, mite-, mouse-, and cat-specific IgE levels were associated with higher FENO concentrations, poorer lung function, and higher blood eosinophils. Higher cat, dust mite, and mouse allergen-specific IgE levels were also associated with an increasing risk of exacerbations or hospitalization. Conclusions: Allergen-specific IgE levels were correlated with allergen exposure among sensitized participants, except for cat. Allergen-specific IgE levels were also associated with more severe asthma across a range of clinical and biologic markers. Adjusting for exposure did not provide additional predictive value, suggesting that higher allergen-specific IgE levels may be indicative of both higher exposure and a greater degree of sensitization, which in turn may result in greater asthma severity. [ABSTRACT FROM AUTHOR]

Abstract: Background: A few studies have outlined a possible relationship between an increased body mass index and allergic rhinitis. A single study reported that males with seasonal allergic rhinitis (SAR), evaluated outside the pollen season, had increased serum adiponectin levels. Objective: The aim of this preliminary study was to evaluate the serum adiponectin levels in a cohort of SAR normo-weight patients evaluated during the pollen season, comparing them with SAR patients evaluated out of pollen season and a group of healthy controls. Methods: The study included 137 subjects; 62 SAR patients evaluated in their pollen season, while symptomatic, 41 SAR patients studied out their pollen season, while they were without symptoms, and 34 normal subjects. All subjects were consecutively evaluated. All of them were normo-weight. A skin prick test and blood sampling for assessing serum adiponectin levels were performed in all subjects. Results: After analysing genders separately, symptomatic male patients had significantly higher levels than both symptomless and normal males (p =0.0041 and 0.0001 respectively), symptomatic female patients showed significantly higher levels than both symptomless and normal females (p =0.0001 and 0.0071 respectively). Conclusion: This study provides the preliminary evidence that adiponectin serum levels might depend on allergen exposure in SAR normo-weight patients. [Copyright &y& Elsevier]

Most children with asthma respond to low doses of inhaled corticosteroids, but a few remain symptomatic despite being prescribed the routine usual asthma medications. The first steps are to ensure that the diagnosis is correct and that the inhaled medications are being given regularly with an appropriately used device. If the children continue to be symptomatic, with any or all of chronic symptoms, acute exacerbations, the need for regular oral corticosteroids, or persistent airflow limitation, then they are considered to have problematic, severe asthma. The next step is to perform a detailed evaluation, including a nurse-lead home visit, to determine whether the child has difficult to treat asthma which improves if the basics are got right, or severe, therapy-resistant asthma; the latter group would be candidates for cytokine-specific therapies. If severe, therapy-resistant asthma is the likely issue, then a detailed invasive investigation is performed, including bronchoscopy, bronchoalveolar lavage and endobronchial biopsy, and trial of adherence with a single intramuscular injection of depot triamcinolone. After detailed phenotyping, an individualised treatment plan is determined. Future work will determine the roles of proximal and distal inflammation, as well as the relative importance of intramural (mucosal) and intraluminal infection. The stability of paediatric asthma phenotypes over time is more variable than those of adults, and the implications of a change of phenotype are yet to be determined. [ABSTRACT FROM AUTHOR]

Abstract: Background: Th17 is a subset of T helper lymphocytes exerting inflammatory activities. Recently, it has been reported that serum IL-17 levels are high in patients with severe birch allergy. Aim of the study: It was to compare the cytokine profile and the frequency of peripheral allergen-specific T helper producing IL-17 in patients with allergic rhinitis. Methods: Twelve patients with persistent allergic rhinitis due to pollens and 5 healthy non-allergic subjects were evaluated during the pollen season. Th17 were evaluated by intracellular staining in T cell compartment ex-vivo and after short activation by allergens and control antigens. Results: Ex-vivo PBMNC evaluation showed that allergic patients had higher frequencies of IL-17 producing T cells. Functional analysis after antigen-specific CD4+ T cell expansion demonstrated that allergic patients had higher frequencies of IL-17 producing T cells than normal subjects. Conclusion: This preliminary study contributes to the knowledge concerning the possible role of Th-17 cells in the response to allergens. [Copyright &y& Elsevier]

Abstract: Background: Several studies have outlined a possible relationship between adipokines and respiratory allergic diseases. However, there are no data about a role for adipsin in allergic rhinitis. Objective: The aim of the study was to evaluate the serum adipsin levels in patients with seasonal allergic rhinitis (SAR), subdivided into two sub-groups: treated or not treated with sublingual immunotherapy (SLIT), and in a group of healthy controls. Methods: The study included 110 subjects; i) 24 SLIT-treated SAR patients, ii) 62 untreated SAR patients, and iii) 24 normal subjects. All subjects were consecutively evaluated. A skin prick test and blood sampling for assessing serum adipsin levels were performed in all subjects. Results: Serum adipsin was increased in SAR patients, even though significant only in males. There was also a significant positive association between adipsin and adiponectin. Conclusion: This preliminary study reports that adipsin serum levels may be increased in some SAR patients, but further functional studies should be performed. [Copyright &y& Elsevier]

Background. Due to the multiple factors affecting exhaled nitric oxide (NO) value, physicians are often puzzled by the result of a single measurement in asthmatic patients. Objective. The aim of this prospective transversal study was to evaluate the relative contributions to exhaled NO fraction (FENO) of the commonly considered major NO determinants, i.e., recent symptoms (upper and lower respiratory tract), atopy (prick skin tests and degree of allergic exposure), and treatment (dose of inhaled corticosteroid [ICS]) to know what information gives a single measure. Methods. FENO at 50 mL/s expiratory flow was measured in 199 asthmatic children (141 boys, age: 11.2 years ± 2.5 years). The allergic risk due to pollen exposure (ARPE index) was independently evaluated by the “Reseau National de Surveillance Aerobiologique.” Results. A multivariate analysis of FENO as dependent variable showed that explanatory variables explained 23% of total FENO variance (symptoms > atopy > ICS). In the children without recent symptoms (n = 118), a FENO > 23 ppb predicted atopy (sensitivity 47%, specificity 85%, p = 0.0006). Multiple regression only showed a trend to significance between FENO and the dose of ICS (p = 0.057, r = - 0.19). Incidentally, despite similar dose of ICS, children under fluticasone (mean ± SD, 259 ± 149 μg/day) had lower FENO than those under budesonide (299 ± 195 μg/day) (median [interquartile], 21 ppb [14-42], n = 55 versus 35 ppb [19-47], n = 104; p = 0.007), which may be due to a higher potency of fluticasone. A relationship between FENO and ARPE index was significant in children with exclusive seasonal sensitisation (n = 31, r = 0.48, p = 0.008). Conclusion. Common exhaled NO determinants weakly explain a single value of FENO, which only can confidently predict atopy. [ABSTRACT FROM AUTHOR]

Background: T helper (Th)-17 cells are a subset of T helper lymphocytes that exert regulatory activities. Recently, it has been reported that serum interleukin (IL)-17 levels are high in the most severe cases of birch allergy studied outside the pollen season. Objective: The aim of this study was to investigate a possible relationship between serum IL-17 levels and clinical parameters in patients with allergic rhinitis studied during the pollen season. Methods: In all, 56 patients with persistent pollen-induced allergic rhinitis were evaluated during the pollen season. Serum IL-17 levels were evaluated by enzyme-linked immunosorbent assay. Symptoms were assessed by visual analogue scale, drug use was monitored and peripheral eosinophils were counted. Results: Serum IL-17 levels were significantly related to clinical symptoms, drug use and peripheral eosinophil counts ( P = 0.0001 for all). Conclusion: This study provides evidence that serum IL-17 level assessment might be considered to classify allergy severity. [ABSTRACT FROM AUTHOR]

Background: An artificial exposure chamber (OHIO Chamber), which allows dispersal of a fixed concentration of Japanese cedar (JC) pollen under stable conditions, was constructed. This study was conducted to identify the exposure conditions assuring validity of the clinical tests conducted using this chamber. Methods: Twenty-four adult patients with JC pollinosis were exposed to different concentrations of JC pollen: 0 (only during the summer period), 4,000, 8,000 and 12,000 grains/m3, and the nasal and ocular symptoms were self-assessed during a 4-hour period of exposure. The amount of nasal discharge was measured and the sneezing frequency was recorded. This study was conducted twice during the summer and winter periods, i.e. non-pollen seasons. The reproducibility of the symptoms between the two seasons was assessed. Results: None of the subjects developed any symptom at the pollen concentration of 0 grains/m3. No significant differences in the time to the onset of symptoms were found between the summer and winter study, regardless of the pollen concentration. There were no significant differences between the summer and winter study in the total symptom score and total nasal symptom score at any pollen concentration, suggesting the very favorable reproducibility of symptoms. Conclusions: Efficient and reproducible results are obtained in patients exposed to JC pollen in the OHIO Chamber. The results suggest the conditions of JC pollen exposure have scientific validity and the OHIO Chamber has the potential to contribute significantly to basic and clinical studies of JC pollinosis. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Copyright of Revue Francaise d'Allergologie is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Subjects with severe and unstable asthma are at high risk of fatal asthma attack. We describe a case of fatal childhood asthma in an 11-year old girl whose asthma was apparently stable with supranormal lung function and identify additional characteristics that should be considered as increasing the risk for fatal asthma. This opportunity was provided by this girl's participation in the Isle of Wight Whole Population Birth Cohort Study. Prospectively collected data identified her as an early-onset persistent wheezer with significant allergic comorbidity. She was highly atopic with multiple allergen sensitization and a total IgE exceeding 5000 Ku/L (normal range: 0-180 ku/l) at 10 years. Additionally at that age, whilst possessing normal lung function (FEV1 2.15 Litres; 110% predicted), she was found to have marked bronchial hyper-responsiveness (PC20 Methacholine 1.71 mg/ml). At the age of 11 years, despite apparent clinical stability and use of regular controller asthma therapy, she suffered a fatal acute asthma attack that may have been related to acute allergen exposure. This report provides further insight into factors associated with fatal childhood asthma. We propose that highly atopic children with early onset persistent asthma are at a higher risk of fatal asthma even if their asthma is apparently stable and lung function is normal. Marked bronchial hyper-responsiveness provides a clue and should be assessed if there is concern. [ABSTRACT FROM AUTHOR]

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Chronic obstructive pulmonary disease (COPD) is conventionally thought of as a disease of adult smokers, related to airway inflammation and structural airway changes (remodeling). However, there is important epidemiological evidence, from a series of studies with overlapping age groups from birth to late middle age that early life events, including antenatal influences on lung growth, program the child to be at increased risk for future COPD. This paper reviews the evidence for potential gene: environment interactions in this process, in particular with respect to the maternal genotype of the COPD patient. It explores the hypothesis that genes important in early lung development are also important in determining adult risk for COPD. Although the major preventable factor adversely impacting on child lung health is maternal smoking, the effects of viral infection, nutrition, and indoor and outdoor pollution are reviewed. The survivors of preterm birth are another important cohort who may develop premature COPD in adult life. Early life events provide the substrate for COPD, with later cigarette smoking, and occasionally other exposures, pulling the trigger to produce COPD. Although a rigorous anti-smoking program is necessary to halt this spiral of lung destruction leading to COPD, a focus on early (including prenatal) lung health is also important. Any model of COPD which does not take into account early life influences is likely to be fatally flawed. [ABSTRACT FROM AUTHOR]