Atopic Status Research Articles

Atopic status and latex sensitization in a cohort of 1,628 students of health care faculties

BackgroundAtopic diseases have increased since the second half of the previous century. Atopic workers are at higher risk to be sensitized to latex, and the first years of exposure are supposed to be especially risky. ObjectiveTo assess atopic status and rate of latex sensitization in health care students starting their exposure to latex gloves. MethodsWe analyzed medical surveillance data from 1,628 health care students from 2010 to 2016. Students completed a questionnaire focused on their previous and current latex exposure and personal and family histories of allergic diseases; underwent skin prick testing with common allergens and latex extract (and/or total and latex-specific immunoglobulin E in serum); and underwent a medical examination. ResultsSkin prick test results for common inhalant allergens showed that 807 of 1,628 students (49.6%) had atopy. Atopy by skin prick testing was associated with male sex (odds ratio 1.49, 95% confidence interval 1.18–1.86), a personal history of oculorhinitis or asthma (odds ratio 10.22, 95% confidence interval 7.4–14.13), and atopic eczema (odds ratio 1.87, 95% confidence interval 1.05–3.36) at multivariate regression analysis. Eleven students (0.7% of total population) were found to be sensitized to latex and all had atopy. ConclusionDespite the high prevalence of atopy in health care students of Trieste, the latex sensitization rate is very low and comparable to general population. This is reasonably due to the low exposure to latex gloves at the time of the evaluation and to low latex release from the gloves currently used in our hospital.

Obesity disproportionately impacts lung volumes, airflow and exhaled nitric oxide in children.

BackgroundThe current literature focusing on the effect of obesity and overweight on lung function and fraction of exhaled nitric oxide (FeNO) in children, particularly among healthy children of non-European descent, remains controversial. Furthermore, whether the relationship of obesity and overweight with lung function and FeNO in children is modified by atopy is unclear. The objective of this study was to examine the effect of excess weight on lung function parameters and FeNO among Asian children, with a particular focus on exploring the potential effect modification by atopy.MethodsWe investigated the effect of excess weight on lung function and FeNO in a population sample of 1,717 children aged 5 to 18 years and explored the potential modifying effect of atopy.ResultsThere were positive associations of body mass index (BMI) z-score with forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), peak expiratory flow (PEF), and forced expiratory flow at 25–75% (FEF25-75) (all P<0.001), after controlling for confounders. The beta coefficient for FEV1 (0.084) was smaller than that for FVC (0.111). In contrast, a negative association was found between BMI z-score and FEV1/FVC ratio (P<0.001) and FeNO (P = 0.03). A consistent pattern of association for lung function variables was observed when stratifying by atopy. There was a negative association of BMI z-score with FeNO in atopic subjects (P = 0.006), but not in non-atopic subjects (P = 0.46).ConclusionsExcess weight disproportionately impacts lung volumes and airflow in children from the general population, independent of atopic status. Excess weight inversely affects FeNO in atopic but not in non-atopic children.

Increased levels of alveolar and airway exhaled nitric oxide in runners

Aim: The objective of this study was to apply extended NO analysis for measurements of NO dynamics in the lung, divided into alveolar and airway contribution, in amateur runners and marathoners.Methods: The athletes participated in either a marathon or a half marathon. The athletes self-reported their age, weight, height, training distance per week, competing distance, cardio-pulmonary health, atopic status, and use of tobacco. Measurements of exhaled NO (FENO) with estimation of alveolar NO (CANO) and airway flux (JawNO), ventilation, pulse oximetry, and peak flow were performed before, immediately after, and 1 hour after completing the race.Results: At baseline the alveolar NO was higher in amateur runners, 2.9 ± 1.1 ppb (p = 0.041), and marathoners, 3.6 ± 1.9 ppb (p = 0.002), than in control subjects, 1.4 ± 0.5 ppb. JawNO was higher in marathoners, 0.90 ± 0.02 nL s−1 (p = 0.044), compared with controls, 0.36 ± 0.02 nL s−1, whereas the increase in amateur runners, 0.56 ± 0.02 nL s−1, did not attain statistical significance (p = 0.165). Immediately after the race there was a decrease in FENO in both amateur runners and marathoners, whereas CANO and JawNO were decreased in marathoners only.Conclusion: Our results support the view that there is an adaptation of the lung to exercise. Thus strenuous exercise increased both airway and alveolar NO, and this might in turn facilitate oxygen uptake.

Rapid adiposity growth increases risks of new-onset asthma and airway inflammation in children.

We aim to (1) examine the influence of long-term adiposity status/short-term adiposity changes on asthma with high or low fractional exhaled nitric oxide (FeNO), and (2) to determine the differences in long-term adiposity status/short-term adiposity changes on atopy, airway inflammation and pulmonary function. We recruited 2450 fourth- to sixth-grade children from the nationwide Taiwan Children Health Study. Data regarding various adiposity indicators, atopic status, pulmonary function tests and asthma outcomes were collected annually. New-onset asthma was stratified by airway inflammation status using FeNO. The generalized estimating equation was used for analyzing longitudinal relationships between long-term adiposity status/short-term adiposity changes and new-onset asthma. Individual adiposity growth slopes were obtained using a hierarchical linear model to establish the relationships between short-term adiposity changes and asthma among children with high airway inflammation. We found long-term adiposity status predicted childhood asthma with low FeNO, whereas short-term adiposity changes may increase risks of childhood asthma with high FeNO. Long-term adiposity status reduced pulmonary function, whereas short-term adiposity increase were associated with atopic diseases and airway inflammation. Obesity-induced asthma could be mediated by high or low airway inflammation, depending on the velocity of increase in adiposity. Rapid adiposity growth may increase risks of childhood asthma and airway inflammation.

Evaluation of exhaled breath temperature (EBT) as a marker and predictor of asthma exacerbation in children and adolescents

ABSTRACTIntroduction: Noninvasive and easy-to-use tools to monitor airway inflammation in asthma are needed to maintain disease control, particularly in pediatric population. The aim of the study was to evaluate exhaled breath temperature (EBT) in pediatric respiratory clinic setting. Methods: We evaluated 37 children and adolescents with asthma (5–17 years; median: 11 years). The patients were followed up in stable condition and during exacerbations (paired observations in n = 19 subjects). We evaluated medication use, EBT, fractional exhaled nitric oxide (FeNO), spirometry and atopic status of patients. Results: EBT was significantly higher in children with asthma exacerbation {entire group: median [interquartile range (IQR)]: 32.3 [1.1]°C vs. 33.8 [1.7]°C; p < 0.001 and mean ± SD: 33.1 ± 1.0°C vs. 33.6 ± 1.1°C; p = 0.038 for paired observations}. Significant correlation was observed between EBT and FeNO in the entire group (r = 0.22; p = 0.03). No difference was observed in EBT median values in atopic and non-atopic subjects in the entire group (median [IQR]: 32.6 [1.6] vs. 32.7 [2.0]; p = 0.88) and in subgroups. There was no difference in EBT values in patients receiving systemic or inhaled glucocorticosteroids (p = 0.45 and 0.83). There was no significant correlation between EBT and body or room temperature. The only significant predictor of exacerbation in logistic regression model was EBT {aOR = 2.4; 95% [confidence interval (CI)]: 1.4–4.1}. ROC analysis demonstrated applicability of EBT as a marker of asthma exacerbation in children (AUC = 0.748; p < 0.001; cut-off = 33.3°C; sensitivity: 64.3%; specificity: 82.1%). Conclusions: We suggest that EBT may serve as marker and predictor of asthma exacerbation in children. EBT follow-up may be useful in asthma monitoring in children and adolescents.

Specific inhalation challenge: the relationship between response, clinical variables and lung function

IntroductionThe specific inhalation challenge (SIC) is considered the gold standard for the diagnosis of occupational asthma (OA). However, its use is not standardised, and the intensity of exposure is regulated...

Programmed cell death‐1 expression correlates with disease severity and IL‐5 in chronic rhinosinusitis with nasal polyps

Programmed cell death-1 (PD-1) is a negative regulator of T-cell responses. Expression of PD-1 and its ligands PD-L1 and PD-L2 in chronic rhinosinusitis with nasal polyps (CRSwNP) is poorly studied. Expression of PD-1, PD-L1, PD-L2, TGF-β, IL-5, and IL-10 mRNA was measured by real-time quantitative PCR on tissue homogenates of patients with CRSwNP (n=21) and healthy controls (n=21) and on primary epithelial cells. Disease severity was scored using the Lund-Mackay scores of maxillofacial computed tomography (CT) scans. Expression of PD-1 and PD-L1/L2 was evaluated at the cellular and tissue levels (n=6) by flow cytometry and immunohistochemistry. Programmed cell death-1 mRNA expression was increased in tissue homogenates from patients with CRSwNP compared with controls, irrespective of the atopy status. Importantly, expression of PD-1 correlated with the total CT scan scores (r=0.5, P=0.02). Additionally, a significant association was found between PD-1 mRNA and expression of IL-5 mRNA in control nasal tissue (r=0.95, P<0.0001) and in CRSwNP (r=0.63, P=0.002). PD-1 was expressed on different subsets of T cells and CD11b- dendritic cells. Both PD-1 and its ligands were expressed on primary epithelial cells from control nasal tissue and nasal polyp tissue. Higher PD-1 expression was found in CRSwNP than in nasal tissue from controls. This was associated with disease severity and tissue IL-5 expression but unrelated to the patients' atopy status.

Persistent asthma phenotype related with late-onset, high atopy, and low socioeconomic status in school-aged Korean children

BackgroundTreatment guidelines for asthma have been established based on asthma severity; there are limitations in the identification of underlying pathophysiology and prediction of prognosis in heterogeneous phenotypes of asthma. Although the complex interactions between environmental and genetic factors affect the development and progression of asthma, studies on asthma phenotypes considering environmental factors are limited. This study aimed to identify asthma phenotypes using latent class analysis including environmental factors in school-age children.MethodsWe included 235 children (6–8 years) with parent-reported, physician-diagnosed asthma from the Children’s HEalth and Environmental Research (CHEER) study, which is a 4-year prospective follow-up study with 2-year intervals. At every survey, pulmonary function tests, methacholine challenge tests and blood tests with questionnaire were conducted.ResultsFour asthma phenotypes were identified. Cluster 1 (22% of children) was characterized by high prevalence of atopy and mild symptoms; subjects in cluster 2 (17%) consisted of less atopy and normal lung function, but intermittent troublesome; cluster 3 (29%) experienced late-onset atopic troublesome asthma with decreased lung function in combination with low socioeconomic status; and cluster 4 was associated with early-onset and less-atopic infrequent asthma.ConclusionsLate-onset, high atopy, and low socioeconomic status are associated with troublesome persistent asthma phenotype in school-age children. Environmental factors might be implicated in the clinical heterogeneity of asthma. Asthma phenotypes considering diverse factors might be more helpful in the identification of asthma pathogenesis and its prevention.

Maternal house dust mite exposure during pregnancy enhances severity of house dust mite–induced asthma in murine offspring

Atopic status of the mother and maternal exposure to environmental factors are associated with increased asthma risk. Moreover, animal models demonstrate that exposure to allergens in strongly sensitized mothers influences offspring asthma development, suggesting that in utero exposures can influence offspring asthma. However, it is unclear whether maternal exposure to common human allergens such as house dust mite (HDM), in the absence of additional adjuvants, influences offspring asthma development. We sought to determine whether maternal HDM exposure influences asthma development in offspring. Pregnant female mice were exposed to PBS or HDM during pregnancy. Using offspring of PBS- or HDM-exposed mothers, the magnitude of HDM or Aspergillus fumigatus (AF) extract-induced airway hyperresponsiveness (AHR), airway inflammation, immunoglobulin production, TH2-associated cytokine synthesis, and pulmonary dendritic cell activity was assessed. Compared with offspring of PBS-exposed mothers, offspring of HDM-exposed mothers demonstrate increased AHR, airway inflammation, TH2 cytokine production, and immunoglobulin levels and a modest decrease in the phagocytic capacity of pulmonary macrophage populations following HDM exposure. Increased sensitivity to AF-induced airway disease was not observed. Offspring of HDM-exposed B-cell-deficient mothers also demonstrated increased HDM-induced AHR, suggesting that transfer of maternal immunoglobulins is not required. Our data demonstrate that maternal exposure to HDM during pregnancy increases asthma sensitivity in offspring in an HDM-specific manner, suggesting that vertical transmission of maternal immune responses may be involved. These findings have important implications for regulation of asthma risk, and suggest that exposure to HDM in the developed world may have underappreciated influences on the overall prevalence of allergic asthma.

Prevalence, risk factors, and clinical outcomes of atopic and nonatopic asthma among rural children

BackgroundBecause of time and cost constraints, objective classification of atopic and nonatopic asthma has been limited in large epidemiologic studies. However, as we try to better understand exposure-outcome associations and ensure appropriate treatment of asthma, it is important to focus on phenotype-defined asthma classification. ObjectiveTo compare atopic and nonatopic asthma in rural children with regard to risk factors and clinical outcomes. MethodsWe conducted a cross-sectional study in rural Saskatchewan, Canada, in 2011. Parents of 6- to 14-year-old children completed a health and exposure survey. Skin prick tests were completed in a subsample of 529 children. Asthma was based physician diagnosis. Asthma status was defined as no asthma, nonatopic asthma, and atopic asthma. ResultsAsthma prevalence was 14.7% of which 32.1% of cases were atopic. After adjustment, early respiratory illness and a family history of asthma were predictors of childhood asthma, regardless of atopic status (P < .05). Being overweight and having a dog in the home were associated with an increased risk of nonatopic asthma (P < .05). A mother with a history of smoking increased the risk of atopic asthma (P = .01). Compared with those with nonatopic asthma, in the past 12 months, children with atopic asthma were more likely to report a sneezy, runny, or blocked nose or have shortness of breath (odds ratio >2), whereas those with nonatopic asthma were more likely to have parents who missed work (odd ratio >3). Those with nonatopic asthma had significantly lower forced expiratory volume in 1 second compared w2ith those with atopic asthma. ConclusionExposures may contribute differentially to atopic and nonatopic asthma and result in differential clinical presentation or burden. The study of these characteristics is important for etiologic understanding and management decisions.

Impact of Internal and External Factors on EBC-pH and FeNO Changes in Humans Following Challenge with Ethyl Acrylate.

Acute effects of ethyl acrylate exposure at 5 ppm for 4 h include changes of pH in exhaled breath condensate (EBC-pH) and exhaled nitric oxide (FeNO). So far, few data have been reported for atopic persons or the impact of the exposure conditions on biomarkers, e.g., constant versus variable application of irritants. Nine atopic and eighteen healthy volunteers without bronchial hyperresponsiveness were exposed for 4 h to ethyl acrylate concentrations of 0.05 ppm (sham), 5 ppm (constant concentration), and 0-10 ppm (variable, mean concentration of 5 ppm) in an exposure laboratory. A positive atopic status was defined according to specific IgE concentrations to common inhalant allergens (sx1 ≥ 0.35 kU/L). Biomarker levels were assessed before and after challenge and adjusted for levels after sham exposure (net response). Ethyl acrylate at constant, but not at variable concentrations induced a significant change in the net responses of EBC-pH and FeNO. Concerning FeNO, this could be observed only for atopic persons. The changes of biomarker levels were related to their baseline values. Biomarker responses to challenge with ethyl acrylate may be influenced by the patterns of application as well as baseline airway inflammation and atopic status of the volunteers.

Clinical Characteristics of Exacerbation-Prone Adult Asthmatics Identified by Cluster Analysis.

PurposeAsthma is a heterogeneous disease characterized by various types of airway inflammation and obstruction. Therefore, it is classified into several subphenotypes, such as early-onset atopic, obese non-eosinophilic, benign, and eosinophilic asthma, using cluster analysis. A number of asthmatics frequently experience exacerbation over a long-term follow-up period, but the exacerbation-prone subphenotype has rarely been evaluated by cluster analysis. This prompted us to identify clusters reflecting asthma exacerbation.MethodsA uniform cluster analysis method was applied to 259 adult asthmatics who were regularly followed-up for over 1 year using 12 variables, selected on the basis of their contribution to asthma phenotypes. After clustering, clinical profiles and exacerbation rates during follow-up were compared among the clusters.ResultsFour subphenotypes were identified: cluster 1 was comprised of patients with early-onset atopic asthma with preserved lung function, cluster 2 late-onset non-atopic asthma with impaired lung function, cluster 3 early-onset atopic asthma with severely impaired lung function, and cluster 4 late-onset non-atopic asthma with well-preserved lung function. The patients in clusters 2 and 3 were identified as exacerbation-prone asthmatics, showing a higher risk of asthma exacerbation.ConclusionsTwo different phenotypes of exacerbation-prone asthma were identified among Korean asthmatics using cluster analysis; both were characterized by impaired lung function, but the age at asthma onset and atopic status were different between the two.

Asthma: What's new, and what should be old but is not!

Asthma is a common condition, which is commonly, badly diagnosed and badly treated, leading to unnecessary morbidity and even death in childhood, despite which complacency about management at all levels of care persists. Asthma is an umbrella term like anaemia and arthritis and should not be used as an unqualified diagnosis. It is suggested that airway disease should be deconstructed into treatable and untreatable components, such as fixed and variable airflow obstruction and airway inflammation and infection. Every effort should be made to make an objective diagnosis, and treatment should be individualised accordingly. Objective testing for airway inflammation may include determination of atopic status, blood eosinophil count and exhaled nitric oxide; physiological testing includes peak flow measurement, comprising response to exercise and short-acting μ-2 agonists. Most school-age atopic children with recurrent wheeze respond well to low-dose inhaled corticosteroids if these are regularly and correctly administered. The provision of an asthma plan is mandatory. If response is poor, rather than uncritically escalating therapies, a review of adherence and any adverse environmental factor should be considered. Asthma attacks are a red flag sign of a bad prognosis, and should prompt a full review, and changes in the asthma plan as necessary. Also, regular reviews of progress and treatment need are mandatory, even in the well child with asthma. In all contexts, the importance of getting the basic rights cannot be overemphasised; still, asthma deaths are attributed to neglect of this principle. Other issues discussed in this review include the approach to the child who is breathless on exercise and the diagnosis of exercise-induced laryngeal obstruction; the so-called habit/honk cough; the problem of breathlessness and airway disease in the obese child, including the airway as the target of systemic inflammation; and the problem of 'asthma' complicating other airways diseases such as cystic fibrosis and extrapulmonary diseases such as sickle-cell anaemia. Overall, the main message of this review is that it should never be forgotten that asthma is a disease which kills children and should always be taken seriously.

Peripheral blood T-helper cells and eosinophil populations in patients with atopic and nonatopic chronic rhinosinusitis.

Analysis of recent research indicated that T-helper cells may play an important role in the pathogenesis of chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP). The purpose of this study was to investigate the peripheral blood Th1 and Th2 cells and eosinophil population in patients with CRS. Peripheral blood samples were obtained from nine nonatopic controls, 37 patients with CRSsNP, and 66 patients with CRSwNP. The samples were then analyzed by flow cytometry analysis (Th1 cell [CD4+, interleukin 4-, interferon γ+]; and Th2 cell [CD4+, interleukin 4+, interferon γ-]). The patients were stratified into four groups based on their allergic status by using skin-prick test results and immunoglobulin E level measurements as the following: (1) nonatopic CRSsNP, (2) nonatopic CRSwNP, (3) atopic CRSsNP, and (4) atopic CRSwNP. Eosinophil counts were also compared. The severity of nasal diseases in these patients was assessed via the Lund-Mackay score. No significant differences in peripheral blood Th1 and Th2 cells were found among all the atopic, nonatopic CRS groups, and the nonatopic control groups. Peripheral blood eosinophil levels in atopic CRSwNP were significantly elevated compared with the nonatopic controls (p < 0.05), but no significant difference was found among all atopic and nonatopic CRS groups. Analysis of our data demonstrated that a proportion of systemic Th1- and Th2-skewed lymphocytes in all CRS groups were similar to that in healthy subjects, irrespective of atopic status. The patients with CRSwNP and with atopy but not the patients with CRSsNP and with atopy demonstrated systemic eosinophilic inflammation. Further studies are needed to investigate underlying pathophysiologic mechanism or endotypes.

Cross-sectional study on allergic sensitization of Austrian adolescents using molecule-based IgE profiling.

Allergen-specific IgE antibodies are a hallmark of type I allergy. The aim of this cross-sectional study was to analyze the sensitization profiles of an Austrian adolescent population utilizing molecule-based IgE diagnosis. Serum samples of 501 nonselected pupils from Salzburg, Austria, were tested in ImmunoCAP ISAC® for IgE reactivity to 112 single allergens. Sensitization profiles were assessed and statistically coordinated with reported allergies. In the population aged 12-21 years, 53.5% showed IgE reactivity to at least one allergen tested. The highest prevalence was found for Phl p 1 from grass pollen (26.5%), group 2 mite allergens (18.2%), Bet v 1 from birch pollen (16.3%) and Fel d 1 from cat (14.4%). The majority of participants showed a complex sensitization profile and reacted on average to 9 allergens. Pollen sensitization was highly prevalent (41.7%) and mainly driven by group I grass and PR-10 allergens of the Betulaceae family, while Pla l 1 represented the most relevant weed. Diagnosed and self-reported allergies were noted in 21.9% and 45.5% of participants, respectively, and correlated well with in vitro results. Among atopic individuals, 71.4% reported to suffer from at least one allergy; concordance was found for grass and cat sensitization, while venom- and weed pollen-positive individuals were frequently asymptomatic. More than half of the tested adolescent population had already established an atopic status presenting a complex IgE reactivity profile dominated by pollen sensitization. Detailed molecule-based analysis allows determining relevant biomarkers and monitoring of the atopic status in populations.

The relationship between biomarkers of fungal allergy and lung damage in asthma.

Immunological biomarkers are the key to the diagnosis of allergic bronchopulmonary aspergillosis (ABPA) and fungal sensitisation, but how these relate to clinically relevant outcomes is unclear. To assess how fungal immunological biomarkers are related to fixed airflow obstruction and radiological abnormalities in moderate to severe asthma. Cross-sectional study of 431 asthmatics. Inflammatory biomarkers, lung function and an IgE fungal panel to colonising filamentous fungi, yeasts and fungal aeroallergens were measured. CT scans were scored for the presence of radiological abnormalities. Factor analysis informed the variables used in a k-means cluster analysis. Fixed airflow obstruction and radiological abnormalities were then mapped to these immunological variables in the cluster analysis. 329 (76.3%) subjects were sensitised to ≥ 1 fungi. Sensitisation to Aspergillus fumigatus and/or Penicillium chrysogenum was associated with a lower post-bronchodilator FEV1 compared with those not sensitised to fungi ((73.0 (95% CI 70.2-76) vs. 82.8 (95% CI 78.5-87.2)% predicted, P < 0.001), independent of atopic status (P = 0.005)), and an increased frequency of bronchiectasis (54.5%, P < 0.001), tree-in-bud (18.7%, P < 0.001) and collapse/consolidation (37.5%, P = 0.002). Cluster analysis identified three clusters: (i) hypereosinophilic (n = 71, 16.5%), (ii) high immunological biomarker load and high frequency of radiological abnormalities (n = 34, 7.9%) and (iii) low levels of fungal immunological biomarkers (n = 326, 75.6%). IgE sensitisation to thermotolerant filamentous fungi, in particular A. fumigatus but not total IgE, is associated with fixed airflow obstruction and a number of radiological abnormalities in moderate to severe asthma. All patients with IgE sensitisation to A. fumigatus are at risk of lung damage irrespective of whether they meet the criteria for ABPA.

Different roles of Staphylococcus aureus enterotoxin in different subtypes of nasal polyps.

Chronic rhinosinusitis with nasal polyps (CRSwNP) is a multifactorial disease. The pathogenesis of CRSwNP remains unclear. This study was designed to investigate the role of inflammation and Staphylococcus aureus enterotoxin (SE) in this disease. The study included a total of 74 patients with CRSwNP and 6 controls. A serum Phadiatop assay was conducted to detect atopy status, and serum eosinophil cationic protein (ECP) and total immunoglobulin (Ig)E levels were determined using ELISA. SEA, SEB, total IgE, ECP and myeloperoxidase (MPO) levels in nasal tissue supernatant were measured using ELISA. The results indicated that 15 (22.1%) patients had systemic allergies. On the basis of the ECP/MPO ratio, the patients were divided into an eosinophilic CRSwNP group (n=18) and a non-eosinophilic CRSwNP group (n=56). The total ECP/MPO ratio was 0.572, with a notable bias toward neutrophilic inflammation. The supernatant ECP and MPO levels were elevated in the CRSwNP group compared with the control group, but no significant difference in the serum total IgE and ECP levels were observed between the CRSwNP and control groups. In addition, the non-eosinophilic and eosinophilic CRSwNP groups showed significant elevations in supernatant total IgE, SEA and SEB levels compared with the control group. Thus, it may be concluded that allergy is a common pathogenesis of CRSwNP, and neutrophilic inflammation is present in most Chinese CRSwNP patients. Additionally, local indicators reflect the inflammatory status more accurately than do serum indicators. SEs may act as an infection factor rather than as a superantigen in Chinese non-eosinophilic CRSwNP patients. Thus, long-term antibiotic therapy may be an option for Chinese non-eosinophilic CRSwNP patients.

Sputum pentraxin 3 as a candidate to assess airway inflammation and remodeling in childhood asthma.

Pentraxin 3 (PTX3) is a soluble pattern recognition receptor and an acute-phase protein. It has gained attention as a new biomarker reflecting tissue inflammation and damage in a variety of diseases. Aim of this study is to investigate the role of PTX3 in childhood asthma.In total, 260 children (140 patients with asthma and 120 controls) were enrolled. PTX3 levels were measured in sputum supernatants using enzyme-linked immunosorbent assay test. We performed spirometry and methacholine challenge tests and measured the total eosinophil count and the serum levels of total IgE and eosinophil cationic protein (ECP) in all subjects.Sputum PTX3 concentration was significantly higher in children with asthma than in control subjects (P < 0.001). Furthermore, sputum PTX3 levels correlated with atopic status and disease severity among patients with asthma. A positive significant correlation was found between sputum PTX3 and the bronchodilator response (r = 0.25, P = 0.013). Sputum PTX3 levels were negatively correlated with forced expiratory volume in 1 second (FEV1) (r = -0.30, P = 0.001), FEV1/forced vital capacity (FVC) (r = -0.27, P = 0.002), and FEF25–75 (r = -0.392, P < 0.001), which are indicators of airway obstruction and inflammation. In addition, the PTX3 concentration in sputum showed negative correlations with post-bronchodilator (BD) FEV1 (r = -0.25, P < 0.001) and post-BD FEV1/FVC (r = -0.25, P < 0.001), which are parameters of persistent airflow limitation reflecting airway remodeling.Sputum PTX3 levels increased in children with asthma, suggesting that PTX3 in sputum could be a candidate molecule to evaluate airway inflammation and remodeling in childhood asthma.

Exhaled nitric oxide in a middle-aged Icelandic population cohort

The prevalence of atopy and asthma is relatively low in Iceland. The purpose of this study was to describe exhaled nitric oxide (FeNO) levels in the general population in correlation with demographic characteristics, smoking status, asthma, rhinitis, atopic status and lung function tests. Altogether 403 subjects, from the European Community Respiratory Health Survey (ECRHS) III who answered the main questionnaire and were checked by FeNO measurements, lung function testing, skin prick testing and measurement of total IgE and specific IgE were included. The geometric mean (95% CI) of FeNO was 16.2 ppb (15.2–17.1) and the prevalence of higher FeNO (⩾25 ppb) was 19.5% in the random sample. Subjects with higher FeNO levels were less likely to be current smokers and more likely to have asthma and rhinitis. Having higher FeNO values was also associated with higher total IgE, having specific IgE to at least one allergen and being skin prick test positive. Current smokers had significantly lower levels of FeNO, geometric mean (95% CI) 9.6 ppb (8.4–11.0), than ex-smokers 18.2 ppb (16.6–20.0) and never smokers 17.3 ppb (16.1–18.5). In multivariable models, having asthma (OR (95% CI) 2.10 (1.20–3.67)), having a specific IgE (OR 2.30 (1.25–4.23)) and being skin prick test positive (OR 2.06 (1.18–3.60)) were independently positively associated with a higher FeNO (⩾25) whereas current smoking was independently negatively associated with a higher FeNO (OR 0.19 (0.06–0.63)). Higher levels of FeNO (⩾25 ppb) were found in one out of five Icelanders; FeNO was positively associated with asthma and allergy and negatively with smoking.

A dynamic landscape of allergen associations in delayed-type cutaneous hypersensitivity.

Delayed-type hypersensitivity represents a significant clinical and public health challenge. Patients undergoing patch testing may exhibit positive reactions to more than one allergen. It is recognized that reactions to specific pairs of allergens are associated, reflecting a combination of exposure patterns and structural similarity. To explore the influence of time of testing, age, sex and atopy status on allergen pair associations in a series of 45 110 consecutive patients tested over 30 years. Patch test records of all patients undergoing testing with a modified European baseline series between 1985 and 2014 were retrieved from a database at St John's Institute of Dermatology. Reactions were read on days 2 and 4. For each allergen it was recorded whether the allergen was tested and whether the result was positive or negative. This is the largest reported study of patch test allergen pair relationships. Our analysis shows a high degree of variability in allergen pair associations. Rigorous statistical analysis reveals a large number of differences between groups, including a significant increase in the association between formaldehyde and multiple formaldehyde-releasing preservatives over the study period, in addition to pair associations with cobalt and formaldehyde-releasing preservatives. These were present to a significantly greater extent in men than in women. These observations extend our understanding of cutaneous allergy, with implications for both clinical practice and mechanisms of cutaneous hypersensitivity.