The Korean journal of internal medicine

The Korean Association of Internal Medicine (대한내과학회)
권호 표지
DOI QR코드

DOI QR Code

Proteomic differences with and without ozone-exposure in a smoking-induced emphysema lung model

  • Uh, Soo-Taek (Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Seoul Hospital) ;
  • Koo, So-My (Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Seoul Hospital) ;
  • Jang, An Soo (Genome Research Center for Allergy and Respiratory Disease, Soonchunhyang University Bucheon Hospital) ;
  • Park, Sung Woo (Genome Research Center for Allergy and Respiratory Disease, Soonchunhyang University Bucheon Hospital) ;
  • Choi, Jae Sung (Division of Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Cheonan Hospital) ;
  • Kim, Yong-Hoon (Division of Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Cheonan Hospital) ;
  • Park, Choon Sik (Genome Research Center for Allergy and Respiratory Disease, Soonchunhyang University Bucheon Hospital)
  • Received : 2014.05.13
  • Accepted : 2014.09.25
  • Published : 2015.01.01
⟨ Previous Next ⟩

Abstract

Background/Aims: Acute exacerbations in chronic obstructive pulmonary disease may be related to air pollution, of which ozone is an important constituent. In this study, we investigated the protein profiles associated with ozone-induced exacerbations in a smoking-induced emphysema model. Methods: Mice were divided into the following groups: group I, no smoking and no ozone (NS + NO); group II, no smoking and ozone (NS + O); group III, smoking and no ozone (S + NO); and group IV, smoking and ozone (S + O). Bronchoalveolar lavage, the mean linear intercept (MLI) on hematoxylin and eosin staining, nano-liquid chromatography-tandem mass spectrometry (LC-MS/MS), and Western blotting analyses were performed. Results: The MLIs of groups III (S + NO) and IV (S + O) ($45{\pm}2$ and $44{\pm}3{\mu}m$, respectively) were significantly higher than those of groups I (NS + NO) and II (NS + O) ($26{\pm}2$ and$23{\pm}2{\mu}m$, respectively; p < 0.05). Fourteen spots that showed significantly different intensities on image analyses of two-dimensional (2D) protein electrophoresis in group I (NS + NO) were identified by LC-MS/MS. The levels of six proteins were higher in group IV (S + O). The levels of vimentin, lactate dehydrogenase A, and triose phosphate isomerase were decreased by both smoking and ozone treatment in Western blotting and proteomic analyses. In contrast, TBC1 domain family 5 (TBC1D5) and lamin A were increased by both smoking and ozone treatment. Conclusions: TBC1D5 could be a biomarker of ozone-induced lung injury in emphysema.

Keywords

Acknowledgement

Supported by : Ministry of Health

References

  1. Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management and Prevention of COPD 2011 [Internet]. [place unknown]: Global Initiative for Chronic Obstructive Lung Disease, 2013 [cited 2013 Dec 15]. Available from: http:// www.goldcopd.org/.
  2. Chapman KR, Mannino DM, Soriano JB, et al. Epidemiology and costs of chronic obstructive pulmonary disease. Eur Respir J 2006;27:188-207. https://doi.org/10.1183/09031936.06.00024505
  3. Kim DS, Kim YS, Jung KS, et al. Prevalence of chronic obstructive pulmonary disease in Korea: a population- based spirometry survey. Am J Respir Crit Care Med 2005;172:842-847. https://doi.org/10.1164/rccm.200502-259OC
  4. Patil SP, Krishnan JA, Lechtzin N, Diette GB. In-hospital mortality following acute exacerbations of chronic obstructive pulmonary disease. Arch Intern Med 2003;163:1180-1186. https://doi.org/10.1001/archinte.163.10.1180
  5. Ai-Ping C, Lee KH, Lim TK. In-hospital and 5-year mortality of patients treated in the ICU for acute exacerbation of COPD: a retrospective study. Chest 2005;128:518-524. https://doi.org/10.1378/chest.128.2.518
  6. Berkius J, Nolin T, Mardh C, Karlstrom G, Walther SM; Swedish Intensive Care Registry. Characteristics and long-term outcome of acute exacerbations in chronic obstructive pulmonary disease: an analysis of cases in the Swedish Intensive Care Registry during 2002-2006. Acta Anaesthesiol Scand 2008;52:759-765. https://doi.org/10.1111/j.1399-6576.2008.01632.x
  7. Medina-Ramon M, Zanobetti A, Schwartz J. The effect of ozone and PM10 on hospital admissions for pneumonia and chronic obstructive pulmonary disease: a national multicity study. Am J Epidemiol 2006;163:579-588. https://doi.org/10.1093/aje/kwj078
  8. Ko FW, Tam W, Wong TW, et al. Temporal relationship between air pollutants and hospital admissions for chronic obstructive pulmonary disease in Hong Kong. Thorax 2007;62:780-785. https://doi.org/10.1136/thx.2006.076166
  9. Halonen JI, Lanki T, Tiittanen P, Niemi JV, Loh M, Pekkanen J. Ozone and cause-specific cardiorespiratory morbidity and mortality. J Epidemiol Community Health 2010;64:814-820. https://doi.org/10.1136/jech.2009.087106
  10. Ciencewicki J, Trivedi S, Kleeberger SR. Oxidants and the pathogenesis of lung diseases. J Allergy Clin Immunol 2008;122:456-468. https://doi.org/10.1016/j.jaci.2008.08.004
  11. Barnes PJ. Alveolar macrophages as orchestrators of COPD. COPD 2004;1:59-70. https://doi.org/10.1081/COPD-120028701
  12. Gerritsen WB, Asin J, Zanen P, van den Bosch JM, Haas FJ. Markers of inflammation and oxidative stress in exacerbated chronic obstructive pulmonary disease patients. Respir Med 2005;99:84-90. https://doi.org/10.1016/j.rmed.2004.04.017
  13. Cazzola M, MacNee W, Martinez FJ, et al. Outcomes for COPD pharmacological trials: from lung function to biomarkers. Eur Respir J 2008;31:416-469. https://doi.org/10.1183/09031936.00099306
  14. Lomas DA, Silverman EK, Edwards LD, et al. Serum surfactant protein D is steroid sensitive and associated with exacerbations of COPD. Eur Respir J 2009;34:95-102. https://doi.org/10.1183/09031936.00156508
  15. Magi B, Bini L, Perari MG, et al. Bronchoalveolar lavage fluid protein composition in patients with sarcoidosis and idiopathic pulmonary fibrosis: a two-dimensional electrophoretic study. Electrophoresis 2002;23:3434-3444. https://doi.org/10.1002/1522-2683(200210)23:19<3434::AID-ELPS3434>3.0.CO;2-R
  16. Larsen K, Malmstrom J, Wildt M, et al. Functional and phenotypical comparison of myofibroblasts derived from biopsies and bronchoalveolar lavage in mild asthma and scleroderma. Respir Res 2006;7:11. https://doi.org/10.1186/1465-9921-7-11
  17. Haque R, Umstead TM, Freeman WM, Floros J, Phelps DS. The impact of surfactant protein-A on ozone-induced changes in the mouse bronchoalveolar lavage proteome. Proteome Sci 2009;7:12. https://doi.org/10.1186/1477-5956-7-12
  18. Luthje L, Raupach T, Michels H, et al. Exercise intolerance and systemic manifestations of pulmonary emphysema in a mouse model. Respir Res 2009;10:7. https://doi.org/10.1186/1465-9921-10-7
  19. Cha MH, Rhim T, Kim KH, Jang AS, Paik YK, Park CS. Proteomic identification of macrophage migration-inhibitory factor upon exposure to $TiO_2$ particles. Mol Cell Proteomics 2007;6:56-63. https://doi.org/10.1074/mcp.M600234-MCP200
  20. Shevchenko A, Wilm M, Vorm O, Mann M. Mass spectrometric sequencing of proteins silver-stained polyacrylamide gels. Anal Chem 1996;68:850-858. https://doi.org/10.1021/ac950914h
  21. Wang D, Wang Y, Liu YN. Experimental pulmonary infection and colonization of Haemophilus influenzae in emphysematous hamsters. Pulm Pharmacol Ther 2010;23:292-299. https://doi.org/10.1016/j.pupt.2010.02.006
  22. Triantaphyllopoulos K, Hussain F, Pinart M, et al. A model of chronic inflammation and pulmonary emphysema after multiple ozone exposures in mice. Am J Physiol Lung Cell Mol Physiol 2011;300:L691-L700. https://doi.org/10.1152/ajplung.00252.2010
  23. Kierstein S, Poulain FR, Cao Y, et al. Susceptibility to ozone-induced airway inflammation is associated with decreased levels of surfactant protein D. Respir Res 2006;7:85. https://doi.org/10.1186/1465-9921-7-85
  24. Williams AS, Nath P, Leung SY, et al. Modulation of ozone-induced airway hyperresponsiveness and inflammation by interleukin-13. Eur Respir J 2008;32:571-578. https://doi.org/10.1183/09031936.00121607
  25. Seaman MN, Harbour ME, Tattersall D, Read E, Bright N. Membrane recruitment of the cargo-selective retromer subcomplex is catalysed by the small GTPase Rab7 and inhibited by the Rab-GAP TBC1D5. J Cell Sci 2009;122(Pt 14):2371-2382. https://doi.org/10.1242/jcs.048686
  26. Shimi T, Pfleghaar K, Kojima S, et al. The A- and B-type nuclear lamin networks: microdomains involved in chromatin organization and transcription. Genes Dev 2008;22:3409-3421. https://doi.org/10.1101/gad.1735208
  27. Valenca SS, de Souza da Fonseca A, da Hora K, Santos R, Porto LC. Lung morphometry and MMP-12 expression in rats treated with intraperitoneal nicotine. Exp Toxicol Pathol 2004;55:393-400. https://doi.org/10.1078/0940-2993-00322
  28. Wright JL, Cosio M, Churg A. Animal models of chronic obstructive pulmonary disease. Am J Physiol Lung Cell Mol Physiol 2008;295:L1-L15. https://doi.org/10.1152/ajplung.90200.2008
  29. Szabari MV, Parameswaran H, Sato S, Hantos Z, Bartolak- Suki E, Suki B. Acute mechanical forces cause deterioration in lung structure and function in elastase-induced emphysema. Am J Physiol Lung Cell Mol Physiol 2012;303:L567-L574. https://doi.org/10.1152/ajplung.00217.2012
  30. Liu ZB, Song NN, Geng WY, et al. Orexin-A and respiration in a rat model of smoke-induced chronic obstructive pulmonary disease. Clin Exp Pharmacol Physiol 2010;37:963-968. https://doi.org/10.1111/j.1440-1681.2010.05411.x
  31. Duan MC, Zhong XN, Huang Y, He ZY, Tang HJ. Mechanisms and dynamics of Th17 cells in mice with cigarette smoke-induced emphysema. Zhonghua Yi Xue Za Zhi 2011;91:1996-2000.
  32. Manoli SE, Smith LA, Vyhlidal CA, et al. Maternal smoking and the retinoid pathway in the developing lung. Respir Res 2012;13:42. https://doi.org/10.1186/1465-9921-13-42
  33. Churg A, Wang RD, Tai H, Wang X, Xie C, Wright JL. Tumor necrosis factor-alpha drives 70% of cigarette smoke-induced emphysema in the mouse. Am J Respir Crit Care Med 2004;170:492-498. https://doi.org/10.1164/rccm.200404-511OC
  34. Churg A, Wang RD, Xie C, Wright JL. alpha-1-Antitrypsin ameliorates cigarette smoke-induced emphysema in the mouse. Am J Respir Crit Care Med 2003;168:199-207. https://doi.org/10.1164/rccm.200302-203OC
  35. Guerassimov A, Hoshino Y, Takubo Y, et al. The development of emphysema in cigarette smoke-exposed mice is strain dependent. Am J Respir Crit Care Med 2004;170:974-980. https://doi.org/10.1164/rccm.200309-1270OC
  36. Cho HY, Gladwell W, Yamamoto M, Kleeberger SR. Exacerbated airway toxicity of environmental oxidant ozone in mice deficient in Nrf2. Oxid Med Cell Longev 2013;2013:254069.
  37. Gunay E, Sarinc Ulasli S, Akar O, et al. Neutrophil-to-lymphocyte ratio in chronic obstructive pulmonary disease: a retrospective study. Inflammation 2014;37:374-380. https://doi.org/10.1007/s10753-013-9749-1

Cited by

  1. Increased neutrophil gelatinase-associated lipocalin (NGAL) promotes airway remodelling in chronic obstructive pulmonary disease vol.131, pp.11, 2015, https://doi.org/10.1042/cs20170096
  2. Identification of differentially expressed proteins in the injured lung from zinc chloride smoke inhalation based on proteomics analysis vol.20, pp.None, 2015, https://doi.org/10.1186/s12931-019-0995-0
  3. Two-hybrid screening of FAM13A protein partners in lung epithelial cells vol.12, pp.None, 2015, https://doi.org/10.1186/s13104-019-4840-9
  4. Effects of Air Pollutants on Airway Diseases vol.18, pp.18, 2021, https://doi.org/10.3390/ijerph18189905