Enhanced levels of prostaglandin E2 and matrix metalloproteinase-2 correlate with the severity of airflow limitation in stable COPD

Background and objective: Cyclooxygenase‐2 (COX‐2) and its product prostaglandin E2 (PGE2) have been demonstrated to play critical roles in inflammation in respiratory diseases. However, the role of COX‐2 in airway remodelling in COPD remains to be elucidated. Matrix metalloproteinase‐2 (MMP‐2) is...

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Vydané v:	Respirology (Carlton, Vic.) Ročník 13; číslo 7; s. 1014 - 1021
Hlavní autori:	CHEN, Yan, CHEN, Ping, HANAOKA, Masayuki, DROMA, Yunden, KUBO, Keishi
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	Melbourne, Australia Blackwell Publishing Asia 01.11.2008
Predmet:	airflow limitation airway remodelling Airway Resistance - physiology Asthma - diagnosis Asthma - metabolism Asthma - physiopathology Blotting, Western COPD Cyclooxygenase 2 - biosynthesis cyclooxygenase-2 Dinoprostone - biosynthesis Enzyme-Linked Immunosorbent Assay Female Follow-Up Studies Forced Expiratory Volume - physiology Humans Male Matrix Metalloproteinase 2 - biosynthesis matrix metalloproteinase-2 Middle Aged prostaglandin E2 Severity of Illness Index Sputum - chemistry Time Factors
ISSN:	1323-7799, 1440-1843, 1440-1843
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Abstract	Background and objective: Cyclooxygenase‐2 (COX‐2) and its product prostaglandin E2 (PGE2) have been demonstrated to play critical roles in inflammation in respiratory diseases. However, the role of COX‐2 in airway remodelling in COPD remains to be elucidated. Matrix metalloproteinase‐2 (MMP‐2) is associated with both inflammation and airway remodelling in COPD. The objective of this study was to measure the expression of COX‐2 and the concentrations of PGE2 and MMP‐2, and to investigate the role of COX‐2 and PGE2 in airflow limitation mediated by MMP‐2, in the pathogenesis of COPD. Methods: Forty‐three patients with stable COPD, twelve smoking control subjects and ten non‐smoking control subjects were enrolled. Induced sputum was obtained for measurement of the concentrations of PGE2 and MMP‐2 by ELISA. COX‐2 protein expression was assessed by western blotting. Results: PGE2 and MMP‐2 concentrations were significantly higher in both smoking control subjects and patients with COPD than in non‐smoking control subjects (P < 0.01). Moreover, the levels of PGE2 and MMP‐2 were inversely correlated with FEV1% predicted in COPD patients (PGE2: r = −0.748, P < 0.01; MMP‐2: r = −0.801, P < 0.01). Levels of PGE2 were also positively correlated with those of MMP‐2 in patients with COPD (r = 0.775, P < 0.01). Expression of COX‐2 protein was significantly higher in COPD patients than in non‐smoking control subjects. Conclusions: COX‐2 and its product PGE2 are not only involved in airway inflammation, but may also contribute to the severity of airflow limitation mediated by MMP‐2 during progression of COPD.
AbstractList	Cyclooxygenase-2 (COX-2) and its product prostaglandin E2 (PGE2) have been demonstrated to play critical roles in inflammation in respiratory diseases. However, the role of COX-2 in airway remodelling in COPD remains to be elucidated. Matrix metalloproteinase-2 (MMP-2) is associated with both inflammation and airway remodelling in COPD. The objective of this study was to measure the expression of COX-2 and the concentrations of PGE2 and MMP-2, and to investigate the role of COX-2 and PGE2 in airflow limitation mediated by MMP-2, in the pathogenesis of COPD. Forty-three patients with stable COPD, twelve smoking control subjects and ten nonsmoking control subjects were enrolled. Induced sputum was obtained for measurement of the concentrations of PGE2 and MMP-2 by ELISA. COX-2 protein expression was assessed by western blotting. PGE2 and MMP-2 concentrations were significantly higher in both smoking control subjects and patients with COPD than in non-smoking control subjects (P < 0.01).Moreover, the levels of PGE2 andMMP-2 were inversely correlated with FEV1%predicted in COPD patients (PGE2: r = -0.748, P < 0.01; MMP-2: r = -0.801, P < 0.01). Levels of PGE2 were also positively correlated with those of MMP-2 in patients with COPD (r = 0.775, P < 0.01). Expression of COX-2 protein was significantly higher in COPD patients than in non-smoking control subjects. COX-2 and its product PGE2 are not only involved in airway inflammation, but may also contribute to the severity of airflow limitation mediated by MMP-2 during progression of COPD. Background and objective: Cyclooxygenase‐2 (COX‐2) and its product prostaglandin E2 (PGE2) have been demonstrated to play critical roles in inflammation in respiratory diseases. However, the role of COX‐2 in airway remodelling in COPD remains to be elucidated. Matrix metalloproteinase‐2 (MMP‐2) is associated with both inflammation and airway remodelling in COPD. The objective of this study was to measure the expression of COX‐2 and the concentrations of PGE2 and MMP‐2, and to investigate the role of COX‐2 and PGE2 in airflow limitation mediated by MMP‐2, in the pathogenesis of COPD. Methods: Forty‐three patients with stable COPD, twelve smoking control subjects and ten non‐smoking control subjects were enrolled. Induced sputum was obtained for measurement of the concentrations of PGE2 and MMP‐2 by ELISA. COX‐2 protein expression was assessed by western blotting. Results: PGE2 and MMP‐2 concentrations were significantly higher in both smoking control subjects and patients with COPD than in non‐smoking control subjects (P < 0.01). Moreover, the levels of PGE2 and MMP‐2 were inversely correlated with FEV1% predicted in COPD patients (PGE2: r = −0.748, P < 0.01; MMP‐2: r = −0.801, P < 0.01). Levels of PGE2 were also positively correlated with those of MMP‐2 in patients with COPD (r = 0.775, P < 0.01). Expression of COX‐2 protein was significantly higher in COPD patients than in non‐smoking control subjects. Conclusions: COX‐2 and its product PGE2 are not only involved in airway inflammation, but may also contribute to the severity of airflow limitation mediated by MMP‐2 during progression of COPD. Cyclooxygenase-2 (COX-2) and its product prostaglandin E2 (PGE2) have been demonstrated to play critical roles in inflammation in respiratory diseases. However, the role of COX-2 in airway remodelling in COPD remains to be elucidated. Matrix metalloproteinase-2 (MMP-2) is associated with both inflammation and airway remodelling in COPD. The objective of this study was to measure the expression of COX-2 and the concentrations of PGE2 and MMP-2, and to investigate the role of COX-2 and PGE2 in airflow limitation mediated by MMP-2, in the pathogenesis of COPD.BACKGROUND AND OBJECTIVECyclooxygenase-2 (COX-2) and its product prostaglandin E2 (PGE2) have been demonstrated to play critical roles in inflammation in respiratory diseases. However, the role of COX-2 in airway remodelling in COPD remains to be elucidated. Matrix metalloproteinase-2 (MMP-2) is associated with both inflammation and airway remodelling in COPD. The objective of this study was to measure the expression of COX-2 and the concentrations of PGE2 and MMP-2, and to investigate the role of COX-2 and PGE2 in airflow limitation mediated by MMP-2, in the pathogenesis of COPD.Forty-three patients with stable COPD, twelve smoking control subjects and ten nonsmoking control subjects were enrolled. Induced sputum was obtained for measurement of the concentrations of PGE2 and MMP-2 by ELISA. COX-2 protein expression was assessed by western blotting.METHODSForty-three patients with stable COPD, twelve smoking control subjects and ten nonsmoking control subjects were enrolled. Induced sputum was obtained for measurement of the concentrations of PGE2 and MMP-2 by ELISA. COX-2 protein expression was assessed by western blotting.PGE2 and MMP-2 concentrations were significantly higher in both smoking control subjects and patients with COPD than in non-smoking control subjects (P < 0.01).Moreover, the levels of PGE2 andMMP-2 were inversely correlated with FEV1%predicted in COPD patients (PGE2: r = -0.748, P < 0.01; MMP-2: r = -0.801, P < 0.01). Levels of PGE2 were also positively correlated with those of MMP-2 in patients with COPD (r = 0.775, P < 0.01). Expression of COX-2 protein was significantly higher in COPD patients than in non-smoking control subjects.RESULTSPGE2 and MMP-2 concentrations were significantly higher in both smoking control subjects and patients with COPD than in non-smoking control subjects (P < 0.01).Moreover, the levels of PGE2 andMMP-2 were inversely correlated with FEV1%predicted in COPD patients (PGE2: r = -0.748, P < 0.01; MMP-2: r = -0.801, P < 0.01). Levels of PGE2 were also positively correlated with those of MMP-2 in patients with COPD (r = 0.775, P < 0.01). Expression of COX-2 protein was significantly higher in COPD patients than in non-smoking control subjects.COX-2 and its product PGE2 are not only involved in airway inflammation, but may also contribute to the severity of airflow limitation mediated by MMP-2 during progression of COPD.CONCLUSIONSCOX-2 and its product PGE2 are not only involved in airway inflammation, but may also contribute to the severity of airflow limitation mediated by MMP-2 during progression of COPD.
Author	CHEN, Ping DROMA, Yunden CHEN, Yan HANAOKA, Masayuki KUBO, Keishi
Author_xml	– sequence: 1 givenname: Yan surname: CHEN fullname: CHEN, Yan organization: Division of Respiratory Disease, Department of Internal Medicine, The Second Xiangya Hospital, Central-South University, Changsha, Hunan, China, and – sequence: 2 givenname: Ping surname: CHEN fullname: CHEN, Ping email: chenping101@hotmail.com organization: Division of Respiratory Disease, Department of Internal Medicine, The Second Xiangya Hospital, Central-South University, Changsha, Hunan, China, and – sequence: 3 givenname: Masayuki surname: HANAOKA fullname: HANAOKA, Masayuki organization: First Department of Medicine, Shinshu University School of Medicine, Matsumoto, Japan – sequence: 4 givenname: Yunden surname: DROMA fullname: DROMA, Yunden organization: First Department of Medicine, Shinshu University School of Medicine, Matsumoto, Japan – sequence: 5 givenname: Keishi surname: KUBO fullname: KUBO, Keishi organization: First Department of Medicine, Shinshu University School of Medicine, Matsumoto, Japan
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References_xml	– reference: Desouza IA, Franco-Penteado CF, Camargo EA, Lima CS, Teixeira SA et al. Acute pulmonary inflammation induced by exposure of the airways to staphylococcal enterotoxin type B in rats. Toxicol. Appl. Pharmacol. 2006; 217: 107-13. – reference: Rabe KF, Hurd S, Anzueto A, Barnes PJ, Buist SA et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary. Am. J. Respir. Crit. Care Med. 2007; 176: 532-55. – reference: Ito H, Duxbury M, Benoit E, Clancy TE, Zinner MJ et al. Prostaglandin E2 enhances pancreatic cancer invasiveness through an Ets-1-dependent induction of matrix metalloproteinase-2. Cancer Res. 2004; 64: 7439-46. – reference: Betsuyaku T, Nishimura M, Takeyabu K, Tanino M, Venge P et al. Neutrophil granule proteins in bronchoalveolar lavage fluid from subjects with subclinical emphysema. Am. J. Respir. Crit. Care Med. 1999; 159: 1985-91. – reference: Pizzichini E, Pizzichini MM, Leigh R, Djukanovic R, Sterk PJ. Safety of sputum induction. Eur. Respir. J. Suppl. 2002; 37: 9s-18s. – reference: Lapperre TS, Willems LN, Timens W, Rabe KF, Hiemstra PS et al. Small airways dysfunction and neutrophilic inflammation in bronchial biopsies and BAL in COPD. Chest 2007; 131: 53-9. – reference: Xaubet A, Roca-Ferrer J, Pujols L, Ramírez J, Mullol J et al. Cyclooxygenase-2 is up-regulated in lung parenchyma of chronic obstructive pulmonary disease and down-regulated in idiopathic pulmonary fibrosis. Sarcoidosis Vasc. Diffuse Lung Dis. 2004; 21: 35-42. – reference: Cataldo D, Munaut C, Noel A, Frankenne F, Bartsch P et al. MMP-2- and MMP-9-linked gelatinolytic activity in the sputum from patients with asthma and chronic obstructive pulmonary disease. Int. Arch. Allergy Immunol. 2000; 123: 259-67. – reference: Willemse BW, Ten Hacken NH, Rutgers B, Lesman-Leegte IG, Postma DS et al. Effect of 1-year smoking cessation on airway inflammation in COPD and asymptomatic smokers. Eur. Respir. J. 2005; 26: 835-45. – reference: Baraldo S, Bazzan E, Zanin ME, Turato G, Garbisa S et al. Matrix metalloproteinase-2 protein in lung periphery is related to COPD progression. Chest 2007; 132: 1733-40. – reference: Adamson IY, Vincent R, Bakowska J. Differential production of metalloproteinases after instilling various urban air particle samples to rat lung. Exp. Lung Res. 2003; 29: 375-88. – reference: Cataldo DD, Gueders MM, Rocks N, Sounni NE, Evrard B et al. Pathogenic role of matrix metalloproteases and their inhibitors in asthma and chronic obstructive pulmonary disease and therapeutic relevance of matrix metalloproteases inhibitors. Cell. Mol. Biol. 2003; 49: 875-84. – reference: Ohnishi K, Takagi M, Kurokawa Y, Satomi S, Konttinen YT. Matrix metalloproteinase-mediated extracellular matrix protein degradation in human pulmonary emphysema. Lab. 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Snippet	Background and objective: Cyclooxygenase‐2 (COX‐2) and its product prostaglandin E2 (PGE2) have been demonstrated to play critical roles in inflammation in... Cyclooxygenase-2 (COX-2) and its product prostaglandin E2 (PGE2) have been demonstrated to play critical roles in inflammation in respiratory diseases....
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SubjectTerms	airflow limitation airway remodelling Airway Resistance - physiology Asthma - diagnosis Asthma - metabolism Asthma - physiopathology Blotting, Western COPD Cyclooxygenase 2 - biosynthesis cyclooxygenase-2 Dinoprostone - biosynthesis Enzyme-Linked Immunosorbent Assay Female Follow-Up Studies Forced Expiratory Volume - physiology Humans Male Matrix Metalloproteinase 2 - biosynthesis matrix metalloproteinase-2 Middle Aged prostaglandin E2 Severity of Illness Index Sputum - chemistry Time Factors
Title	Enhanced levels of prostaglandin E2 and matrix metalloproteinase-2 correlate with the severity of airflow limitation in stable COPD
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