ABSTRACT
To determine if asthma control was more difficult to achieve in obese versus non-obese asthmatic children, retrospective analysis was performed on obese and non-obese Los Angeles inner-city children (2 to 18 years of age) with persistent asthma. No difference in time required to achieve control of asthma, ability to maintain control of asthma, baseline pulmonary functions, and number of controllers prescribed was found between the two groups. We conclude that in a Los Angeles inner-city pediatric population, obesity is not a factor in the ability to control asthma.
Subject(s)
Asthma/therapy , Obesity/complications , Adolescent , Anti-Asthmatic Agents/therapeutic use , Asthma/complications , Asthma/physiopathology , Body Mass Index , Child , Child, Preschool , Female , Humans , Infant , Male , Obesity/physiopathology , Respiratory Function Tests , SpirometryABSTRACT
Deficient expression of the counterregulatory cytokine IL-10 by lung inflammatory cells may facilitate chronic inflammation and the pathogenesis of hyaline membrane disease (HMD), in premature infants. To determine if pathways which regulate proinflammatory cytokines in response to human recombinant IL-10 (rIL-10) were functional in the lungs of these neonates, bronchoalveolar lavage (BAL)-derived lung inflammatory cells (predominantly macrophages and neutrophils) from infants with HMD were cultured in the presence of lipopolysaccharide (LPS) and increasing concentrations of (rIL-10). The expression of IL-1beta and IL-8 protein was assessed 24 h later. IL-10 protein was also measured from the BAL aspirates of these newborns at 4-day intervals over the first month of life. In cell culture IL-1beta expression was inhibited by rIL-10 in a dose-dependent fashion while IL-8 expression was inhibited by higher concentrations of rIL-10. IL-10 protein was undetectable from BAL fluid of the premature infants sampled over 28 days. The results demonstrate that lung inflammatory cells, which do not express IL-10 in vivo, are capable of responding to rIL-10 in cell culture with reduction of IL-1beta and IL-8 expression. These data support the rationale for the development of rIL-10 as a potential anti-inflammatory agent in the treatment of HMD.
