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Background: Asthma and obstructive sleep apnea (OSA) often coexists during childhood. To delineate this clinical association, we investigated the phenotypical features of OSA in asthmatic children. Specifically, we hypothesized that asthmatic children have a distinct OSA phenotype that involves a higher prevalence of Rapid-Eye-Movement (REM)-related breathing abnormalities relative to children with OSA alone., Methods: We conducted a retrospective cross-sectional analysis of 141 children aged 2-12 years with OSA diagnosed by polysomnography (PSG) in our sleep center. Outcomes included PSG parameters, maximal %SaO2 REM desaturations and prevalence of REM-related OSA. Multivariate linear regression model or logistic regression model was built to study the joint effect of asthma and OSA parameters with control for potential confounders (significance level P < 0.05)., Results: Baseline respiratory parameters, obstructive apnea-hypopnea index (OAHI) severity, and oxygenation during NREM sleep were unaffected by the presence of asthma in children with OSA. In contrast, maximal %SaO2 REM desaturation, REM-OAHI and prevalence of REM-related OSA in children with moderate-severe OSA were significantly increased in asthmatic children with OSA compared to subjects with OSA alone. Multivariate analysis revealed that the association between asthma and REM-related OSA parameters is independent of asthma control, BMI, age, and gender. The presence of REM-related OSA in asthmatics was unaffected by rhinitis or atopic status., Conclusion: These results demonstrate that asthma is associated with REM-related breathing abnormalities in children with moderate-severe OSA. The link between asthma and REM-related OSA is independent of asthma control and obesity. Further research is needed to delineate the REM-sleep biological mechanisms that modulate the phenotypical expression of OSA in asthmatic children., (Copyright © 2012 Wiley Periodicals, Inc.)

The prevalence of maternal obesity has increased dramatically with adverse consequences on infant health. Prior studies have reported associations between maternal obesity and childhood wheeze, asthma as well as lower respiratory tract infections (LRTI). However, studies examining the association of obesity with early-life LRTIs in low-income urban minority populations are still lacking. This is a critical gap because both obesity and infant respiratory morbidity are more prevalent and severe in these communities. We examined mother‐child dyads from the Boston Birth Cohort (BBC) to define the longitudinal association of maternal pre‐pregnancy BMI and LRTI in infancy, defined as the presence of bronchiolitis, bronchitis, or pneumonia during the first year of life (< 12 months of age). A total of 2,790 mother‐child dyads were included in our analyses. Infants born to pre-pregnancy obese mothers (n = 688, 25%) had 1.43 increased odds (adjOR = 1.43, 95% CI 1.08–1.88, p = 0.012) of developing LRTI during the first year of life when compared with newborns born to normal-weight mothers after adjusting by relevant LRTI risk factors. Notably, infants born to overweight mothers (n = 808, 29%) followed a similar trend (adjOR = 1.31, 95% CI 1.00–1.72, p = 0.048). Our study demonstrated that maternal pre-pregnancy obesity is an independent risk factor for the development of LRTI during infancy in a low-income urban minority birth cohort. [ABSTRACT FROM AUTHOR]

Over the past two decades, several studies have positioned early-life microbial exposure as a key factor for protection or susceptibility to respiratory diseases. Birth cohorts have identified a strong link between neonatal bacterial colonization of the nasal airway and gut with the risk for respiratory infections and childhood asthma. Translational studies have provided companion mechanistic insights on how viral and bacterial exposures in early life affect immune development at the respiratory mucosal barrier. In this review, we summarize and discuss our current understanding of how early microbial--immune interactions occur during infancy, with a particular focus on the emergent paradigm of "innate immune training". Future human-based studies including newborns and infants are needed to inform the timing and key pathways implicated in the development, maturation, and innate training of the airway immune response, and how early microbiota and virus exposures modulate these processes in the respiratory system during health and disease. [ABSTRACT FROM AUTHOR]