Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
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ISSN 1899–5276 (print), ISSN 2451-2680 (online)
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Advances in Clinical and Experimental Medicine

2007, vol. 16, nr 2, March-April, p. 277–285

Publication type: review article

Language: Polish

Patogeneza przewlekłej obturacyjnej choroby płuc – udział komórek i cytokin w procesie zapalnym

Pathogenesis of Chronic Obstructive Pulmonary Disease – the Role of Cells and Mediators in Chronic Inflammation

Małgorzata Król1,, Maria Kraus−Filarska1,, Andrzej Obojski1,

1 Department of Internal Medicine and Allergology, Silesian Piasts University of Medicine in Wrocław, Poland

Streszczenie

Przewlekła obturacyjna choroba płuc (p.o.ch.p.) jest chorobą zapalną dróg oddechowych i miąższu płucnego. Zapalenie rozwija się w wyniku nieprawidłowej odpowiedzi płuc na działanie dymu tytoniowego i innych szkodliwych gazów i pyłów. Przewlekły proces zapalny prowadzi do uszkodzenia tkanek, nieprawidłowej odbudowy, a nawet do nieodwracalnego zniszczenia płuc. Choroba jest przewlekła i postępująca, jej przebieg jednak może być zahamowany przez zaprzestanie palenia tytoniu lub ekspozycji na inne toksyczne gazy i pyły. W artykule omówiono szczegółowo mechanizmy rozwoju zapalenia, rolę dymu tytoniowego, a także udział i znaczenie poszczególnych komórek i mediatorów w procesie zapalnym.

Abstract

Chronic obstructive pulmonary disease (COPD) is characterised by chronic inflammation throughout the airways and parenchyma. Chronic inflammation results from abnormal inflammatory response of lungs to cigarette smoke and other inhaled noxious particles and gases. The inflammation leads to tissue damage, repair mechanisms disruption and finally to irreversible lung destruction. The disease is chronic and progressive but their course can be stopped by smoking cessation or reduction of exposure to other noxious particles or gases. In this article mechanisms of chronic inflammation, the role of cigarette smoke and the role of inflammatory cells and their mediators in the chronic inflammation are discussed.

Słowa kluczowe

przewlekła obturacyjna choroba płuc, patogeneza, zapalenie, komórki zapalne, cytokiny

Key words

chronic obstructive pulmonary disease, pathogenesis, inflammation, inflammatory cells, cytokines

References (44)

  1. Celli BR, MacNee W: and committee members. Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS/ERS position paper: Eur Respir J 2004, 23, 932–946.
  2. Światowa strategia rozpoznawania, leczenia i prewencji przewlekłej obturacyjnej choroby płuc. Aktualizacja 2006. Med Prakt 2/2007 (wydanie specjalne).
  3. Kozielski J, Chazan R, Górecka D, Jahnz−Różyk K, Jędrychowski W, Kuna P, Małolepszy J, Pierzchała W, Pirożyński M, Płusa T, Słomiński JM, Śliwiński P, Zieliński J: Zalecenia Polskiego Towarzystwa Ftyzjopneumonologicznego rozpoznawania i leczenia przewlekłej obturacyjnej choroby płuc (p.o.ch.p.). Pneumonol Alergol Pol 2002, 70, supl. 2.
  4. Hogg JC: Pathophysiology of airway inflammation in chronic obstructive pulmonary disease. Lancet 2004, 364, 709–721.
  5. Saetta M, Turato G, Maestrelli P, Mapp CE, Fabbbri LM: Cellular and structural bases of chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2001, 163, 1304–1309.
  6. Shapiro SD, Ingenito EP: The pathogenesis of chronic obstructive pulmonary disease. Advances in the past 100 years. Am J Respir Cell Mol Biol 2005, 32, 367–372.
  7. Willemse BWM, ten Hacken NHT, Rutgers SR, Lesman−Leegte IGAT, Postma DS, Timens W: Effect of 1−year smoking cessation on airway inflammation in COPD and asymptomatic smokers. Eur Respir J 2005, 26, 835–845.
  8. Rutgers SR, Postma DS., ten Hacken NH, Kauffman HF, van Der Mark TW, Koeter GH, Timens W: Ongoing inflammation in patients with COPD who do not currently smoke. Thorax 2000, 55, 12–18.
  9. Mróz RM, Szulakowski P, Pierzchała W, Chyczewska E, MacNee W: Patogeneza przewlekłej obturacyjnej choroby płuc. Część I. Podłoże komórkowe. Wiad Lek 2006, 59, 92–96.
  10. Bhowmik A, Seemungal TAR, Sapsford RJ, Wedzicha JA: Relation of sputum inflammatory markers to symptoms and lung function changes in COPD exacerbations. Thorax 2000, 55, 114–120.
  11. Di Stefano A, Capelli A, Lusuardii M, Balbo P, Vecchio C, Maestrelli P, Mapp CE, Fabbri LM, Donner CF, Saetta M: Severity of airflow inflammation is associated with severity of airway inflammation in smokers. Am J Respir Crit Care Med 1998, 158, 1277–1285.
  12. O’Donnell R, Breen, Wilson S, Djukanovich R: Inflammatory cells in the airways in COPD. Thorax 2006, 61, 448–454.
  13. Tetley TD: Macrophages and the pathogenesis of COPD. Chest 2002, 121, 156–159.
  14. Cosio MG, Majo J, Cosio MG: Inflammation of the airways and lung parenchyma in COPD. Role of T cells. Chest 2002, 121, 160–165.
  15. Stockley RA: Neutrophils and the pathogenesis of COPD. Chest 2002, 121, 151–155.
  16. O’Donnell RA, Peebles C, Ward JA, Daraker A, Angco G, Proberg P, Pierrou S, Lund J, Holgate ST, Davies DE, Delany DJ, Wilson SJ, Djukanovich R: Relationship between peripheral airway disfunction, airway obstruction and neutrophilic inflammation in COPD. Thorax 2004, 59, 837–842.
  17. MacNee W: Oxidative stres and lung inlammation in airways disease. Eur J Pharmacol 2001, 429, 195–207.
  18. Prescott E, Bjerg AM, Andersen PK, Lange P, Vestbo J: Gender difference in smoking effects on lung function and risk of hospitalization for COPD: results from Danish longitudinal population study. Eur Respir J 1997, 10, 822–827.
  19. Barnes PJ, Shapiro SD, Pauwels RA: Chronic obstructive pulmonary disease: molecular and cellular mechanism. Eur Respir J 2003, 22, 672–688.
  20. Barnes PJ: Chronic obstructive pulmonary disease. NEJM 2000, 343, 269–280.
  21. Barnes PJ: Alveolar macrophages as orchestrator of COPD. COPD 2004, 1, 59–70.
  22. Lomas DA, Silverman EK: The genetics of chronic obstructive pulmonary disease. Respir Res 2001, 2, 20–26.
  23. Barnes PJ: Reduced histone deacetylase in COPD. Clinical implications. Chest 2006, 129, 151–155.
  24. Pryor WA, Stone K: Oxidants in cigarette smoke. Radicals, hydrogen peroxide, peroxynitrate and peroxynitrite. Ann NY Acad Sci 1993, 686, 12–27.
  25. Rennard SI: Overview of causes of COPD. Przyczyny przewlekłej obturacyjnej choroby płuc. Lepsze zrozumienie patogenezy i patomechanizmów choroby pozwala opracować nowe sposoby leczenia. Med Dypl 2002, 11, 62–74.
  26. Willemse BW, Postma DS, Timens W, ten Hacken NHT: The impact of smoking cessation on respiratory symptoms, lung function, airway hyperresponsiveness and inflammation. Eur Respir J 2004, 23, 464–476.
  27. Pesci A, Balbi B. Majori M, Cacciani G, Bertacco S, Alciato P et al.: Inflammatory cells and mediators in bronchial lavage of patients with chronic obstructive pulmonary disease. Eur Respir J 1998, 12, 380–386.
  28. Peleman RA, Rytila PH, Kips JC, Joos GF, Pauwels RA: The cellular composition of induced sputum in chronic obstructive pulmonary disease. Eur Respir J 1999, 13, 839–843.
  29. Finkelstein R, Fraser RS, Ghezzo H, Cosio MG: Alveolar inflammation and its relation to emphysema in smokers. Am J Respir Crit Care Med 1995, 152, 1666–1672.
  30. Di Stefano A, Caramori G, Oates T, Capelli A, Lusuardi M, Gnemmi I, Ioli F, Chung KF, Donner CF, Barnes PJ, Adcock IM: Increased expression of NF−κB in bronchial biopsies from smokers and patients with COPD. Eur Respir J 2002, 20, 556–563.
  31. Wu L, Chau J, Young RP, Pokorny V, Mills GD, Hopkins R, McLean L, Black PN: Transforming growth factor−beta1 genotype and susceptibility to chronic obstructive pulmonary disease. Thorax 2004, 59, 126–129.
  32. Vernooy JHJ, Lindeman JHN, Jacobs JA, Hanemaaijer R, Wouters EFM: Increased activity of matrix metalloproteinase−8 and matrix metalloproteinase−9 in induced sputum from patients with COPD. Chest 2004, 126, 1802–1810.
  33. Shapiro SD: The macrophage in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1999, 160, 29–32.
  34. Lacoste JY, Bousquet J, Chanez P, Van Vyve T, Simony−Lafontaine J et al.: Eosinophilic and neutrophilic inflammation in asthma, chronic bronchitis and chronic obstructive pulmonary disease. J Allergy Clin Immunol 1993, 92, 537–548.
  35. Baraldo S, Turato G, Badin C, Bazzan E, Beghe B, Ziun R, Calabrese F, Casoni G, Maestrelli P, Papi A, Fabbri LM, Saetta M: Neutrophilic infiltration within the airway smooth muscle in patients with COPD. Thorax 2004, 59, 308–312.
  36. Saetta M, Di Stefano A, Maeastrelli P, Ferrareso A, Drigo R, Potena A et al.: Activated T−lymphocytes and macrophages in bronchial mucosa of subjects with chronic bronchitis. Am Rev Respir Dis 1993, 147, 301–306.
  37. O’Shaughnessy TC, Ansari TW, Barnes NC, Jeffery PK: Inflammation in bronchial biopsies of subjects with chronic bronchitis: inverse relationship of CD8+ T lymphocytes with FEV1. Am J Respir Crit Care Med 1997, 155, 852–857.
  38. Saetta M, Baraldo S, Corbino L et al.: CD8+ve cells in the lungs of smokers with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1999, 160, 711–717.
  39. Steinke JW, Borish L: Cytokines and chemokines. J Allergy Clin Immunol 2006, 117, 441–445.
  40. Kemeny DM, Vyas B, Vukmanovic−Stejic M, Thomas MJ, Noble A, Loh Li−Cher, O’Connor BJ: CD8+ T cell subsets and chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1999, 160, 33–37.
  41. Chung KF: Cytokines in chronic obstructive pulmonary disease. Eur Respir J 2001, 18, Suppl. 34, 50–59.
  42. Mueller R, Chanez P, Campbell AM, Bousquet J, Heusser C, Bullock GR: Different cytokine patterns in bronchial biopsies in asthma and chronic bronchitis. Respir Med 1996, 90, 79–85.
  43. Oudijk E−JD, Lammers J−W−J, Koenderman L: Systemic inflammation in chronic obstructive pulmonary disease. Eur Respir J 2003, 22, Suppl. 46, 5–13.
  44. Barnes PJ: Mediators of chronic obstructive pulmonary disease. Pharmacol Rev 2004, 56, 515–548.
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