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박춘식,심은영,박종숙,장안수,박성우,김도진,어수택,김용훈 대한결핵 및 호흡기학회 2013 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.116 No.-
Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive form of lung disease characterized by fibrosis. Epigenetic mechanisms are likely to be associated with pathogenesis in IPF.We compared microarray data of DNA methylation and RNA expression. Methods and Findings: We performed genome-wide DNA methylation and gene expression profiling in a total of 12 samples including 4 IPF-rapid, 4 IPF-slow and 4 adjacent normal lung tissues using the Illumina HumanMethylation450 BeadChip and Illumina HumanHT-12 BeadChip. Genome-wide differences in DNA methylation status and RNA expression were demonstrated by array hybridization. Among 485,577 loci examined, 10,937 site were significantly different between NC and IPF with p<0.01. When the subjects were divided into two groups (rapid vs. slow IPF), the IPF-rapid and normal controls clustered distinctly, and IPF-slow samples were not classified clearly. Among the expression level of the 47,231 curated and putative genes and ESTs, which represent 30,494 unique genes gene, 683 gene showed different expression between NC and IPF with p<0.05. When the subjects were divided into two groups (rapid vs. slow IPF), the IPF-rapid and normal controls clustered distinctly, and IPF-slow samples were not classified clearly. Among the genes whose DNA methylation status and RNA expression were both significantly altered between IPF-rapid and normal controls, 84 genes of the 118 genes were hypermethylated in DNA associated with decreased mRNA expression or vice versa. We further characterized the 84 genes to evaluate their potential biological function and found that the methylation changes could have effect on the bronchiole development with TCF21, HOXA5. Conclusion: The combined analysis of DNA methylation and gene expression identified genes to be involved in IPF, suggesting that DNA methylation is important in the pathogenesis of IPF.Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive form of lung disease characterized by fibrosis. Epigenetic mechanisms are likely to be associated with pathogenesis in IPF.We compared microarray data of DNA methylation and RNA expression. Methods and Findings: We performed genome-wide DNA methylation and gene expression profiling in a total of 12 samples including 4 IPF-rapid, 4 IPF-slow and 4 adjacent normal lung tissues using the Illumina HumanMethylation450 BeadChip and Illumina HumanHT-12 BeadChip. Genome-wide differences in DNA methylation status and RNA expression were demonstrated by array hybridization. Among 485,577 loci examined, 10,937 site were significantly different between NC and IPF with p<0.01. When the subjects were divided into two groups (rapid vs. slow IPF), the IPF-rapid and normal controls clustered distinctly, and IPF-slow samples were not classified clearly. Among the expression level of the 47,231 curated and putative genes and ESTs, which represent 30,494 unique genes gene, 683 gene showed different expression between NC and IPF with p<0.05. When the subjects were divided into two groups (rapid vs. slow IPF), the IPF-rapid and normal controls clustered distinctly, and IPF-slow samples were not classified clearly. Among the genes whose DNA methylation status and RNA expression were both significantly altered between IPF-rapid and normal controls, 84 genes of the 118 genes were hypermethylated in DNA associated with decreased mRNA expression or vice versa. We further characterized the 84 genes to evaluate their potential biological function and found that the methylation changes could have effect on the bronchiole development with TCF21, HOXA5. Conclusion: The combined analysis of DNA methylation and gene expression identified genes to be involved in IPF, suggesting that DNA methylation is important in the pathogenesis of IPF.
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박춘식,배다정,박종숙,장안수,박성우 대한결핵 및 호흡기학회 2013 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.116 No.-
Background: Epigenetics is responsible for the gene - environmental interaction of asthma development. Although Ozone is an important contributor to exacerbation of asthma, the role of epigenetics behind ozone - induced airway dysfunction is not known yet.We investigated trans-generational transmission of ozone - induced airway dysfunction and the underlying epigenetic changes in the lung of animal model. Method: 6 weeks old BALB/C female mice were exposed to filter air or O3 (2 ppm, 3 hr/day, day 1 to day 21). Airway resistance (Pehn), and BAL procedure were performed at weekly interval. mRNA expression of DNMT1, 3a, 3b, MeCP2, MBDs, HDAC3, Chrm1,2,3 and ADRß2 genes were measured in RNA extracted from lung tissue using Real-Time PCR. For trans-generational transmission study, 6weeks old BALB/C female mice (F0) were exposed to filter air (Air-F0) or O3 (1p pm, Ozone-F0) during pregnancy. Pehn was measured at 5 and 6 weeks of age in F1, F2 and F3 mice grown up in filter air, and cytokines (IL-1 alpha, beta, 4, 5, 8, 9, 10, 12, 13, 17, 22, 23) Lipoxin A4, Resolvin E1, Prostaglandin E2 were measured in BALF using ELISA kit. Result: After Ozone exposure, Pehn value was significantly increased in a time dependent manner with concomitant BAL neutrophilia. MBDs and HDAC3 increased at hour 3, while DNMT1, 3a, 3b, MeCP2 started to increase at day 14 and peaked at day 21 of Ozone exposure. In the trans-generational models, F1~ F3 mice born from Ozone-F0 showed persistent elevation of Pehn and BAL neutrophilia. IL-5, 8, 9,10, and 12 elevated in F1 of OzoneF0, but returned in F2 and F3 compared to those of Air F0. DNMT1,3a,3b of Ozone-F0 to Ozone-F3 increased, while Chrm2 and ADRß2 were decreased compared to those of AirF0. Conclusion: Ozone - induced airway dysfunction may be transmitted to F3 generation with altered expression of the genes related with airway function potentially via epigenetic changes.Background: Epigenetics is responsible for the gene - environmental interaction of asthma development. Although Ozone is an important contributor to exacerbation of asthma, the role of epigenetics behind ozone - induced airway dysfunction is not known yet.We investigated trans-generational transmission of ozone - induced airway dysfunction and the underlying epigenetic changes in the lung of animal model. Method: 6 weeks old BALB/C female mice were exposed to filter air or O3 (2 ppm, 3 hr/day, day 1 to day 21). Airway resistance (Pehn), and BAL procedure were performed at weekly interval. mRNA expression of DNMT1, 3a, 3b, MeCP2, MBDs, HDAC3, Chrm1,2,3 and ADRß2 genes were measured in RNA extracted from lung tissue using Real-Time PCR. For trans-generational transmission study, 6weeks old BALB/C female mice (F0) were exposed to filter air (Air-F0) or O3 (1p pm, Ozone-F0) during pregnancy. Pehn was measured at 5 and 6 weeks of age in F1, F2 and F3 mice grown up in filter air, and cytokines (IL-1 alpha, beta, 4, 5, 8, 9, 10, 12, 13, 17, 22, 23) Lipoxin A4, Resolvin E1, Prostaglandin E2 were measured in BALF using ELISA kit. Result: After Ozone exposure, Pehn value was significantly increased in a time dependent manner with concomitant BAL neutrophilia. MBDs and HDAC3 increased at hour 3, while DNMT1, 3a, 3b, MeCP2 started to increase at day 14 and peaked at day 21 of Ozone exposure. In the trans-generational models, F1~ F3 mice born from Ozone-F0 showed persistent elevation of Pehn and BAL neutrophilia. IL-5, 8, 9,10, and 12 elevated in F1 of OzoneF0, but returned in F2 and F3 compared to those of Air F0. DNMT1,3a,3b of Ozone-F0 to Ozone-F3 increased, while Chrm2 and ADRß2 were decreased compared to those of AirF0. Conclusion: Ozone - induced airway dysfunction may be transmitted to F3 generation with altered expression of the genes related with airway function potentially via epigenetic changes.
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Protection of leukotriene receptor antagonist against aspirin-induced bronchospasm in asthmatics
박춘식,박종숙,장안수,박성우,Young Mok Lee,,Yong Hoon Kim,박세민 대한천식알레르기학회 2010 Allergy, Asthma & Immunology Research Vol.2 No.1
Purpose: Leukotriene receptor antagonists (LTRAs) are used to treat aspirin-intolerant asthma (AIA); however, the protective effects of long-term LTRA administration against aspirin-induced bronchospasm have not been evaluated. Objectives: We investigated the efficacy of a 12-week treatment with a LTRA in protecting against aspirin-induced asthma in AIA patients. Methods: Fifty-two adult patients with AIA underwent an aspirin challenge test just before administration of montelukast (10 mg/day) and just after 12 weeks of treatment. The protective effect was assessed as the disappearance of aspirin-induced bronchospasm after 12 weeks of treatment. The results were compared according to the patients’ clinical and physiological parameters. Results: The decline in FEV1 following aspirin challenge was significantly reduced from 28.6±1.9% to 10.2±1.7%(P=0.0001) after 12 weeks of montelukast treatment. However, 14 subjects (30%) still showed a positive response (>15% decline in FEV1) to aspirin challenge. Grouping the subjects into good and poor responders according to post-treatment responses revealed that the pretreatment aspirin-induced FEV1 decline was significantly greater in the poor responders and that the triggering dose of aspirin and the induction time for a positive response were lower and shorter, respectively, in the poor responders. Histories of aspirin hypersensitivity and sinusitis were more prevalent among the poor responders than among the good responders. Conclusions: Twelve weeks of treatment with montelukast protected against aspirin-induced bronchospasm in 70% of the AIA cases. A poor response was associated with more severe aspirin-induced bronchospasms before treatment and a history of aspirin hypersensitivity or sinusitis. Clinical implications: A severe response to aspirin challenge may be a predictor of poor responsiveness to leukotriene antagonist treatment.
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Eosinophilic Bronchitis, Eosinophilia Associated Genetic Variants, and Notch Signaling in Asthma
박춘식 대한천식알레르기학회 2010 Allergy, Asthma & Immunology Research Vol.2 No.3
While much has indeed been learned about the biology and role of eosinophils, the paradigm of eosinophils has the pros and cons in development of asthma. To answer the questions in the black box, this review firstly discusses the biological and morphological differences between asthma and eosinophilic bronchitis (EB). EB is an interesting clinical manifestation of eosinophilic airway disease that does not involve airway hyperresponsiveness (AHR), demonstrating that airway eosinophilia alone is insufficient to merit a diagnosis of asthma. Secondly, I will describe and discuss the effect(s) of single-nucleotide polymorphisms (SNPs) in the genes CCR3, IL-5 RECEPTOR ALPHA (IL5RA), and IL1RL1, and finally the in vitro and in vivo effects of Notch inhibition on both eosinophil differentiation and experimental asthma. Eosinophilic airway inflammation is not as important in the pathogenesis and maintenance of asthma as had previously been thought. However, the role of eosinophils in other asthma subphenotypes, including refractory or severely remodeled asthma, needs to be evaluated further. High-throughput methodologies such as genomics will facilitate the discovery of new markers of inflammation; these, in turn, will aid in the evaluation of the role of eosinophils in asthma and its various subphenotypes.
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Effects of Smoking Cessation on Airflow Obstruction and Quality of Life in Asthmatic Smokers
박춘식,장안수,박성우,Do-Jin Kim,SooTaek Uh,황헌규,Gun Il Lim 대한천식알레르기학회 2010 Allergy, Asthma & Immunology Research Vol.2 No.4
Purpose: Smoking elicits airway inflammation and airflow obstruction in patients with asthma, even after smoking cessation. The aim of this study was to examine the effects of smoking cessation on lung function and quality of life (QOL) in asthmatic patients. Methods: Thirty-two patients with asthma who were active smokers were recruited. After education on the effects of smoking on asthma, 22 patients continued to smoke, and 10 quit smoking. All patients were treated with inhaled fluticasone propionate (1 mg/day) for 3 months. We compared forced expiratory volume in 1 s (FEV1),FEV1/forced vital capacity (FVC), forced expiratory flow between 25 and 75% FVC (FEF25–75%), and scores on a QOL questionnaire at baseline, 1, 2,and 3 months. Results: Quitters showed a greater percent change in FEV1 (19.1±6.3 vs. 7.9±2.4%, P=0.024) and FEV1/FVC (6.5±4.14 vs. 3.5±1.5%, P=0.05) than smokers. Both quitters and smokers showed improved QOL scores after 1, 2, and 3 months of fluticasone treatment. Conclusions:Patients with asthma who quit smoking showed less airway obstruction, suggesting that smoking cessation is crucial in the management of asthma.
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