Supplementary Material for: Exacerbating Factors Induce Different Gene Expression Profiles in Peripheral Blood Mononuclear Cells from Asthmatics, Patients with Chronic Obstructive Pulmonary Disease and Healthy Subjects

<p><b><i>Background:</i></b> Despite several common phenotypic features, chronic obstructive pulmonary disease (COPD) and severe asthma differ with regard to their causative factors and pathophysiology. Both diseases may be exacerbated by environmental factors, however, the molecular profiles of disease episodes have not been comprehensively studied. We identified differences in gene and protein expression profiles expressed by peripheral blood mononuclear cells (PBMC) of COPD patients, patients with atopic asthma and healthy subjects when challenged with exacerbating factors in vitro: lipopolysaccharide (LPS), house dust mite (HDM) and cat allergen. <b><i>Methods:</i></b> PBMC isolated from patients with severe atopic asthma and COPD, as well as healthy subjects were stimulated with rDer p 1 DG, rFel d 1 DG and LPS. The changes in the expression of 47 genes belonging to five groups (phospholipase A₂, eicosanoids, transcription factors, cytokines and airway remodeling) were studied using TaqMan low density array cards. Immunoblotting was used to study relative protein expression. <b><i>Results:</i></b> rDer p 1 significantly up-regulated the expression of <i>PLA2G4A, PLA2G6, PLA2G15, CYSLTR1, LB4R2, PTGS1, PTGS2</i>, <i>FOXP1</i>, <i>GATA3</i>, <i>HDAC2</i>, <i>IREB2</i>, <i>PPARG</i>, <i>STAT4</i>, <i>TSLP </i>and<i> CHI3L1</i> genes in asthmatics in comparison to healthy subjects. LPS induced significant expression of <i>ANXA1</i> and<i> LTA4H </i>in asthmatics when compared to COPD patients and healthy subjects. <i>SOX6,</i><i>STAT4 </i>and <i>IL1RL1 </i>were induced in COPD after LPS stimulation. Analysis of protein expression revealed a pattern similar to mRNA expression. <b><i>Conclusions:</i></b> LPS-induced exacerbation of asthma and COPD is characterized by differential expression of selected genes in PBMC. HDM allergen changed the expression profile of inflammatory genes between patients with asthma of atopic origin and healthy controls.</p

Towards estimating the burden of disease attributable to second-hand smoke exposure in Polish children

Objectives: To estimate the burden of disease attributable to second-hand smoke (SHS) exposure in Polish children in terms of the number of deaths and disability adjusted life years (DALYs) due to lower respiratory infections (LRI), otitis media (OM), asthma, low birth weight (LBW) and sudden infant death syndrome (SIDS). Materials and Methods: Estimates of SHS exposure in children and in pregnant women as well as information concerning maternal smoking were derived from a national survey, the Global Youth Tobacco Survey, and the Global Adult Tobacco Survey in Poland. Mortality data (LRI, OM, asthma, and SIDS), the number of cases (LBW), and population data were obtained from national statistics (year 2010), and DALYs came from the WHO (year 2004). The burden of disease due to SHS was calculated by multiplying the total burden of a specific health outcome (deaths or DALYs) by a population attributable fraction. Results: Using two estimates of SHS exposure in children: 48% and 60%, at least 12 and 14 deaths from LRI in children aged up to 2 years were attributed to SHS, for the two exposure scenarios, respectively. The highest burden of DALYs was for asthma in children aged up to 15 years: 2412, and 2970 DALYs, for the two exposure scenarios, respectively. For LRI, 419 and 500 DALYs, and for OM, 61 and 77 DALYs were attributed to SHS, for the two exposure scenarios, respectively. Between 13% and 27% of SIDS cases and between 3% and 16% of the cases of LBW at term were attributed to SHS exposure. Conclusions: This study provides a conservative estimate of the public health impact of SHS exposure on Polish children. Lack of comprehensive, up to date health data concerning children, as well as lack of measures that would best reflect actual SHS exposure are major limitations of the study, likely to underestimate the burden of disease