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Background: Obesity is a risk factor for asthma. Studies in mice suggest that the adipokines leptin and adiponectin affect asthmatic responses. The purpose of this study was to determine if adipokines associated with obesity are (1) altered in obese women with asthma compared to controls and (2) associated with increased cytokines and chemokines involved in allergic inflammation., Methods: We performed a cross-sectional study of asthmatic and non-asthmatic obese premenopausal women. Participants answered questionnaires and performed lung function tests. Serum and peripheral blood mononuclear cells (PBMCs) were collected for analysis of cytokines and adipokines., Results: A total of 22 asthmatic (mean body mass index 40.0 ± 5.1 kg/m(2)) and 20 non-asthmatic women (mean body mass index 41.3 ± 5.6 kg/m(2)) participated. We found no difference in serum adipokine concentrations between asthmatics and non-asthmatics. Serum adiponectin correlated positively with PBMC eotaxin (r(s) = 0.55, p = .0003) and RANTES (regulated upon activation, normal T-cell expressed, and secreted) (r(s) = 0.36, p = .03), whereas serum leptin correlated negatively with PBMC eotaxin (r(s) = -0.34, p = .04). There was a negative correlation between serum adiponectin and PBMC interferon-γ (r(s) = -0.41, p = .01)., Conclusions: Perturbations of adipokines that occur in obesity were correlated with decreased cytokine production typically associated with allergic responses in PBMC of obese premenopausal women. This study suggests that although obese asthmatics may have elements of Th2-mediated inflammation, adipokine derangements in obesity are associated with Th1 rather than Th2 bias. Obesity has complex effects on allergic inflammation and is likely to be important modifier of the pathogenesis of airway disease in asthma.

Background: Asthma is a chronic inflammatory disease of the airway that is characterized by a Th2-type of immune response with increasing evidence for involvement of Th17 cells. The role of IL-6 in promoting effector T cell subsets suggest that IL-6 may play a functional role in asthma. Classically IL-6 has been viewed as an inflammatory marker, along with TNFalpha and IL-1beta, rather than as regulatory cytokine., Objective: To investigate the potential relationship between IL-6 and other proinflammatory cytokines, Th2/Th17 cytokines and lung function in allergic asthma, and thus evaluate the potential role of IL-6 in this disease., Methods: Cytokine levels in induced sputum and lung function were measured in 16 healthy control and 18 mild-moderate allergic asthmatic subjects., Results: The levels of the proinflammatory biomarkers TNFalpha and IL-1beta were not different between the control and asthmatic group. In contrast, IL-6 levels were specifically elevated in asthmatic subjects compared with healthy controls (p < 0.01). Hierarchical regression analysis in the total study cohort indicates that the relationship between asthma and lung function could be mediated by IL-6. Among Th2 cytokines only IL-13 (p < 0.05) was also elevated in the asthmatic group, and positively correlated with IL-6 levels (rS = 0.53, p < 0.05)., Conclusions: In mild-moderate asthma, IL-6 dissociates from other proinflammatory biomarkers, but correlates with IL-13 levels. Furthermore, IL-6 may contribute to impaired lung function in allergic asthma.

Study Objectives: The purpose of this study was to determine if asthma with rhinitis and asthma without rhinitis represent distinct forms of disease., Design: We performed a prospective cross-sectional study., Participants: The study included healthy controls, participants with asthma without rhinitis, and participants with both asthma and rhinitis. Interventions We compared lung function and airway inflammation between the three groups of participants., Results: We recruited 32 participants: 12 normals, 8 asthmatics without rhinitis, and 12 with rhinitis. Compared to asthmatics with rhinitis, asthmatics without rhinitis had more severe airflow limitation (FEV(1)/FVC = 60.6% [IQR = 22.8] vs. 74.8% [IQR = 7.8] and fewer induced sputum eosinophils (2.8 [IQR = 5.8] and 9.6 [IQR = 23.8], respectively). Sputum interleukin-6 correlated inversely with lung function measured by postbronchodilator FEV(1) in the study cohort (Spearman correlation coefficient = -0.55, p < 0.01)., Conclusions: Asthmatics without rhinitis tend to have lower lung function and less eosinophilic inflammation in the lung. This small study suggests that asthmatics without rhinitis represent a distinct phenotype of asthma in which low lung function is dissociated from eosinophilic cellular inflammation, and it suggests that larger studies addressing this phenotype are warrented.

An indoor air study was conducted during the summers of 2007 and 2008 to determine the effect(s) of resident lifestyle on the concentrations and distributions of volatile organic compounds (VOCs) in residences of the city of Niagara Falls, New York. A GrayWolf Sensing Solutions Total Volatile Organic Compound (TVOC) detector was used to measure TVOC concentrations and generic air readings of five predetermined locations within each of 58 residences. Factors including smoking, asthma, furnace filter condition, pest infestations and air conditioning and their effect(s) on TVOC concentrations were evaluated. The general distributions of TVOC within each residence were determined. Examining the latter three variables revealed no significant differences. However, TVOC concentrations increased as high as 20% in smoking households. Asthmatic households exhibited TVOC levels elevated as high as 33%. Additionally, TVOC levels from smoking households and asthmatic households gave a linear relationship (R2 =0.96). [ABSTRACT FROM AUTHOR]