K. Tomita, G. Caramori, Kazuhiro Ito, Sam Lim, H. Sano, Y. Tohda, I. Adcock, P. Barnes
{"title":"Telomere Shortening in Alveolar Macrophages of Smokers and COPD Patients~!2010-02-18~!2010-03-05~!2010-04-15~!","authors":"K. Tomita, G. Caramori, Kazuhiro Ito, Sam Lim, H. Sano, Y. Tohda, I. Adcock, P. Barnes","doi":"10.2174/1874375701004010023","DOIUrl":null,"url":null,"abstract":"Background: Tobacco smoking is reported to enhance telomere shortening in peripheral blood lymphocytes. However, telomere length of lung resident cells such as alveolar macrophages (AMs) has not been evaluated. Aim: We evaluated effect of tobacco smoking on telomere length in AMs. Methods: AMs were obtained from nine non-smokers (mean age 24.6 years, mean FEV1/FVC 93.8%) and ten healthy smokers (mean age 25.2 years, >10 pack-years, mean FEV1/FVC 90.6%). We also analyzed tissue macrophages from eight moderate to severe COPD patients (mean age 68.3 years, >10 pack-years, mean FEV1/FVC 54.2%, mean %pred. FEV1 48.8%), age-matched nine healthy smokers (mean age 67.1 years, >10 pack- years, mean FEV1/FVC 83.7%, mean % pred. FEV1 82.4%), and eight healthy non-smokers (mean age 71.2 years, mean FEV1/FVC 84.6%, mean %pred. FEV1 84.1%). Centromere signals and telomere length were analysed using quantitative fluorescence in situ hybridization (QFISH) and confocal microscopy. Results: Telomere length was reduced in bronchoalveolar lavage macrophages of younger smokers compared with that observed in healthy non-smoker's AMs, Importantly, there was no quantitative difference in centromere signals between smokers and non-smokers. A shorter telomere length was also seen in tissue macrophages from older smokers with or without COPD compared with non-smokers. However there was no difference in telomere length between healthy smokers and smokers with COPD. Conclusion: Tobacco smoking enhances telomere shortening in AMs from patients with and without COPD.","PeriodicalId":89507,"journal":{"name":"The open pathology journal","volume":"2 1","pages":"23-29"},"PeriodicalIF":0.0000,"publicationDate":"2010-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"12","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The open pathology journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/1874375701004010023","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 12
Abstract
Background: Tobacco smoking is reported to enhance telomere shortening in peripheral blood lymphocytes. However, telomere length of lung resident cells such as alveolar macrophages (AMs) has not been evaluated. Aim: We evaluated effect of tobacco smoking on telomere length in AMs. Methods: AMs were obtained from nine non-smokers (mean age 24.6 years, mean FEV1/FVC 93.8%) and ten healthy smokers (mean age 25.2 years, >10 pack-years, mean FEV1/FVC 90.6%). We also analyzed tissue macrophages from eight moderate to severe COPD patients (mean age 68.3 years, >10 pack-years, mean FEV1/FVC 54.2%, mean %pred. FEV1 48.8%), age-matched nine healthy smokers (mean age 67.1 years, >10 pack- years, mean FEV1/FVC 83.7%, mean % pred. FEV1 82.4%), and eight healthy non-smokers (mean age 71.2 years, mean FEV1/FVC 84.6%, mean %pred. FEV1 84.1%). Centromere signals and telomere length were analysed using quantitative fluorescence in situ hybridization (QFISH) and confocal microscopy. Results: Telomere length was reduced in bronchoalveolar lavage macrophages of younger smokers compared with that observed in healthy non-smoker's AMs, Importantly, there was no quantitative difference in centromere signals between smokers and non-smokers. A shorter telomere length was also seen in tissue macrophages from older smokers with or without COPD compared with non-smokers. However there was no difference in telomere length between healthy smokers and smokers with COPD. Conclusion: Tobacco smoking enhances telomere shortening in AMs from patients with and without COPD.