Study of Bronchial Inflammation in Adolescent Smokers With and Without Obesity
The investigators want to assess differences in lung function and bronchial inflammation of young smokers and non-smokers with (BMI > 30) and without obesity (BMI < 25)(4 patient groups). The aim of the study is to compare differences in lung function (VC, FEV1, VC/FEV1, metacholine challenge) and bronchial inflammation in relation with smoking history and levels of exhaled CO. For the latter the investigators will analyze the levels of IL-8, IL-6, TNF alpha and INF gamma and mRNA of LBP, TLR2 and TLR4 in sputum. Further, inflammatory markers e.g. low CRP and inflammatory cytokines levels in the blood will be investigated. The aim is to describe a early stage of chronic obstructive pulmonary disease caused by cigarette smoke in juvenile smokers, and the relationship between bronchial inflammation and obesity in adolescents.
|Study Design:||Observational Model: Cohort
Time Perspective: Cross-Sectional
|Official Title:||Bronchial Inflammation in Adolescent Smokers With and Without Obesity|
- Bronchial inflammatory in adolescents smokers with and without obesity [ Time Frame: one day ] [ Designated as safety issue: No ]
- Association of bronchial inflammatory parameters in sputum and in the blood [ Time Frame: one day ] [ Designated as safety issue: No ]
Biospecimen Retention: Samples With DNA
serum: total IgE, RAST urin: cotinine, leukotrienes sputum: leukotrienes, white cells whole blood
|Study Start Date:||October 2008|
|Study Completion Date:||February 2010|
|Primary Completion Date:||February 2010 (Final data collection date for primary outcome measure)|
BMI > 30 kg/m2 CO ≥ 15 ppm
BMI < 25 kg/m2 CO ≥ 15 ppm
BMI > 30 kg/m2 CO ≤ 6 ppm
BMI < 25 kg/m2 CO ≤ 6 ppm
Tobacco smoke is the crucial factor at the beginning and in the course of the bronchial inflammation leading to COPD. It has been shown that cigarette smoke in vitro leads to a MAP kinase and NF-κB-dependent increase of pro-inflammatory cytokines, and inhibits bacteria-induced expression of β-defensins. Several studies revealed an increase of inflammatory cytokines like IL-8 and TNF in the sputum of smokers. Further studies demonstrated an up regulation of LTB4 and LBP possibly due to the LPS derived from tobacco smoke. Hasday et al could show that up to 15 ng per cigarette LPS is released. In principle, the cigarette smoke exposure liked a mild LPS inhalation. In separate work, we could show that LPS inhalation in healthy non-smokers to an increase of CRP and LBP concentrations in the serum lead. In another study of adolescents, 24 smokers (age 17.7 years) and 24 non-smoking (age 17.5 years) were compared. The CO in smokers was significantly increased, and the NO concentrations decreased. At the same time there was a significantly greater bronchial hyperreagibility in the smoker group.
According to a recent study in Germany (KiGGS study), already 31% of the adolescents' boys and 32% of the girls do smoke. The social status is of great importance. Boys and girls from families with a low social status smoke more frequently than those from families with middle-and especially with higher social status. Similarly obesity is linked to the social status with overweight occurring more often in families with a lower social status.
A visceral obesity is closely associated with the risk of type-2-diabetes as well as other aspects of the metabolic syndrome. However, the existing insulin resistance is of fundamental importance. Due to increased visceral fat depots and subsequently increased release of proinflammatory proteins various complications do occur.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00942019
|Children's Hospital, Goethe-University|
|Frankfurt/Main, Germany, 60596|
|Principal Investigator:||Stefan Zielen, Prof.||Children´s Hospital, Goethe-University, Frankfurt, Germany|