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Background: This study aimed to (i) assess the prevalence of exposure to environmental tobacco smoke (ETS) at homes, (ii) assess the prevalence of atopic dermatitis and (iii) evaluate the association between ETS exposure and atopic dermatitis status among adolescents.Methods: During October 2015, a cross-sectional study design was implemented using a self-administered, modified version of the ISAAC (International Study of Asthma and Allergies in Childhood) questionnaire among students enrolled in nine high schools of one of the six governorates of Kuwait. Prevalence of ETS exposure at home (1 or more smokers at home vs. none) and atopic dermatitis were computed. A multivariable log-binomial regression model was used to evaluate the adjusted association between ETS exposure and atopic dermatitis.Results: Of 800 invited students, 746 (93.3%) participated, of whom 74.8% were Kuwaiti and 50.1% were female with a mean (SD) age of 16.8 (0.68) years. Prevalence of ETS exposure at home was 54%. Prevalence of atopic dermatitis was 14.9%. A final multivariable log-binomial regression model showed that compared with the adolescents free from atopic dermatitis, adolescents with atopic dermatitis were significantly more likely to have had ETS exposure at home (adjusted prevalence ratio = 1.49; 95% CI: 1.03-2.14; p = 0.034) or tended to be female (adjusted prevalence ratio = 1.42; 95% CI: 0.99-2.03; p = 0.054).Conclusions: A high prevalence of ETS exposure at home among adolescents was recorded. ETS exposure and female gender were significantly associated with atopic dermatitis status. Intervention fostering voluntary adoption of a smoke-free home rule may help protect the adolescents against ETS exposure and alleviate the menace of associated morbidity. [ABSTRACT FROM AUTHOR]

Background: Cockroach (CR) allergens frequently cause severe asthma in CR-sensitized subjects. Allergen-specific immunotherapy causes a shift of allergic Th2 responses towards Th1 and/or regulatory T cell (Treg) responses which reduce airway inflammation and prevent disease progression. Data are relatively limited on immunotherapy via CR allergy vaccine. Methods: The therapeutic efficacy of an intranasal liposome-adjuvant vaccine made of a refined Periplaneta americana arginine kinase (AK) was compared to the liposome-entrapped P. americana crude extract (CRE) vaccine. Adult BALB/c mice were rendered allergic to CRE. Three allergic mouse groups were immunized intranasally on alternate days with 8 doses of liposome-entrapped CRE (L-CRE), liposome-entrapped AK and placebo, respectively. One week later, all mice received a nebulized CRE provocation. Evaluation of vaccine efficacy was performed 1 day after provocation. Results: Liposome-entrapped native AK attenuated airway inflammation after the CRE provocation and caused a shift of allergic Th2 to Th1 and Treg responses. The L-CRE also induced a shift from the Th2 to the Th1 response but did not induce a Treg response and could not attenuate the airway inflammation upon allergen reexposure. Conclusions: Intranasal liposome-adjuvant CR allergy vaccine containing native AK (Per a 9) is better than L-CRE in attenuating allergic airway inflammation. The findings of this study not only document a more comprehensive and beneficial immune response induced by the refined allergen vaccine but also raise the point that the shift from the Th2 to the Th1 response alone might not correlate with improved airway histopathology, clinical outcome and quality of life. Copyright © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

It has been pointed out that obesity is a risk factor for, and is involved in the exacerbation of asthma. Mounting evidence about adipose tissue-derived proteins (adipokines) gave rise to the current understanding of obesity as a systemic inflammatory disorder. In this review, we summarized the involvement of leptin, focusing on eosinophil functions. Several studies have indicated that leptin can restrain eosinophil apoptosis, enhance migration, increase adhesion molecules and induce cytokine production. Since leptin also acts on a variety of immune cells related to allergic response, increased leptin in obese individuals potentially explains the mechanism by which obesity leads to an exacerbation of asthma. Further studies targeting adipokines will delineate the association between obesity and eosinophil-associated diseases. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Experimental data suggest that asthma exacerbation by allergens is enhanced by exposure to environmental tobacco smoke (ETS); however, there is little supporting epidemiologic evidence. To our knowledge, few studies have assessed respiratory symptoms and allergies in this context. Objectives: To evaluate whether the association of exposure to animals (indicators of allergen and endotoxin exposure) with asthma-related symptoms is modified by ETS exposure in Chinese children. Methods: A cross-sectional study of 8,819 children in kindergarten was conducted in 25 districts in northern China. Information on respiratory health and exposure to indoor allergens was obtained using a standard questionnaire from the American Thoracic Society. Results: Among the children with ETS exposure in utero, the effects of exposure to animals were significant with respect to persistent cough [adjusted odds ratio (OR) 1.83; 95% confidence interval (CI) 1.12-2.99] and persistent phlegm (adjusted OR 2.40; 95% CI 1.28-4.54). The combined effect of in utero ETS exposure and animal exposure on doctor-diagnosed asthma was approximately as expected on the basis of their independent effects on an additive scale. There was no interaction between animal exposure and ETS exposure in the first 2 years of life or current ETS exposure. Conclusions: This study provides evidence that animal and ETS exposure increases the risk of asthma-related symptoms in children in kindergarten. ETS exposure in utero did modify the effect of animal exposure on persistent phlegm and persistent cough but not on doctor-diagnosed asthma among children. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]