Proinflammatory cytokines, transforming growth factor-β1, and fibrinolytic enzymes in loculated and free-flowing pleural exudates

Chi L. Chung, Chi Hung Chen, Joen Rong Sheu, Yi C. Chen, Shi Chuan Chang

研究成果: 雜誌貢獻文章

50 引文 (Scopus)

摘要

Study objectives: To measure tumor necrosis factor (TNF) α, interleukin (IL) 1β, and transforming growth factor (TGF) β1 in loculated and free-flowing pleural effusions caused by malignancy, tuberculosis (TB), and pneumonia and their relationship with plasminogen activator inhibitor-type 1 (PAI-1) and tissue-type plasminogen activator (tPA) and to compare the differences between loculated and free-flowing effusions. Design: A prospective study. Patients and methods: The effusion levels of TNF-α, IL-1β, TGF-β1, PAI-1, and tPA were measured in 29 patients with malignant effusions, 19 patients with TB, and 30 patients with parapneumonic effusions. Pleural effusions were divided into loculated and free-flowing groups by imaging studies. A group of 42 patients with loculated effusions was subdivided into primary and secondary loculation groups by chest ultrasonography. Results: The median levels of TNF-α (87.0 pg/mL), IL-1β (13.8 pg/mL), TGF-β1 (10,952.9 pg/mL), PAI-1 (111.2 ng/mL), and lactate dehydrogenase (LDH) [498 IU/dL] in the loculated group were significantly higher than those in the free-flowing group (TNF-α, 15.0 pg/mL; IL-1β, 2.9 pg/mL; TGF-β1, 6,117.3 pg/mL; PAI-1, 61.5 ng/mL, and LDH, 266 IU/dL). In both the loculated and free-flowing effusions, the levels of TGF-β1 correlated positively with those of TNF-αa (r = 0.51 and p <0.001 vs r = 0.42 and p <0.05, respectively) and IL-1β (r = 0.52 and p <0.001 vs r = 0.49 and p <0.01, respectively), and the values of PAI-1 correlated positively with those of TNF-α (r = 0.59 and p <0.001 vs r = 0.55 and p <0.001, respectively), IL-1β (r = 0.35 and p <0.05 vs r = 0.47 and p <0.01, respectively), and TGF-β1 (r = 0.53 and p <0.001 vs r = 0.58 and p <0.001, respectively). In contrast, the levels of tPA correlated negatively with those of TNF-α (r = -0.37, p <0.05) and IL-1β (r =-0.56, p <0.001) in loculated effusions. Twenty-seven of 42 patients with loculated effusions were classified into a secondary loculation group, which, compared with the primary loculation group, had significantly higher median levels of effusion TNF-α (119.2 vs 14.2 pg/mL, respectively; p = 0.001), IL-1β (33.3 vs 3.4 pg/mL, respectively; p <0.001), TGF-β1 (13,152.7 vs 7746.0 pg/mL, respectively; p = 0.041), and PAI-1 (114.9 vs 94.1 pg/mL, respectively; p = 0.019). Conclusion: Compared with free-flowing effusions, fibrinolytic activity was depressed in loculated effusions. A higher intensity of pleural inflammation in loculated effusions may enhance the release of TNF-α, IL-1β, and TGF-β1, which may subsequently increase the levels of PAI-1. The imbalance of PAI-1 and tPA in pleural spaces may lead to fibrin deposition and loculation of pleural effusions.
原文英語
頁(從 - 到)690-697
頁數8
期刊Chest
128
發行號2
DOIs
出版狀態已發佈 - 八月 2005

指紋

Transforming Growth Factors
Exudates and Transudates
Plasminogen Activator Inhibitor 1
Interleukin-1
Tumor Necrosis Factor-alpha
Cytokines
Enzymes
Pleural Effusion
Plasminogen Activators
L-Lactate Dehydrogenase
Tuberculosis
Plasminogen Inactivators
Tissue Plasminogen Activator
Fibrin
Ultrasonography
Pneumonia
Thorax
Prospective Studies
Inflammation

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

引用此文

Proinflammatory cytokines, transforming growth factor-β1, and fibrinolytic enzymes in loculated and free-flowing pleural exudates. / Chung, Chi L.; Chen, Chi Hung; Sheu, Joen Rong; Chen, Yi C.; Chang, Shi Chuan.

於: Chest, 卷 128, 編號 2, 08.2005, p. 690-697.

研究成果: 雜誌貢獻文章

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title = "Proinflammatory cytokines, transforming growth factor-β1, and fibrinolytic enzymes in loculated and free-flowing pleural exudates",
abstract = "Study objectives: To measure tumor necrosis factor (TNF) α, interleukin (IL) 1β, and transforming growth factor (TGF) β1 in loculated and free-flowing pleural effusions caused by malignancy, tuberculosis (TB), and pneumonia and their relationship with plasminogen activator inhibitor-type 1 (PAI-1) and tissue-type plasminogen activator (tPA) and to compare the differences between loculated and free-flowing effusions. Design: A prospective study. Patients and methods: The effusion levels of TNF-α, IL-1β, TGF-β1, PAI-1, and tPA were measured in 29 patients with malignant effusions, 19 patients with TB, and 30 patients with parapneumonic effusions. Pleural effusions were divided into loculated and free-flowing groups by imaging studies. A group of 42 patients with loculated effusions was subdivided into primary and secondary loculation groups by chest ultrasonography. Results: The median levels of TNF-α (87.0 pg/mL), IL-1β (13.8 pg/mL), TGF-β1 (10,952.9 pg/mL), PAI-1 (111.2 ng/mL), and lactate dehydrogenase (LDH) [498 IU/dL] in the loculated group were significantly higher than those in the free-flowing group (TNF-α, 15.0 pg/mL; IL-1β, 2.9 pg/mL; TGF-β1, 6,117.3 pg/mL; PAI-1, 61.5 ng/mL, and LDH, 266 IU/dL). In both the loculated and free-flowing effusions, the levels of TGF-β1 correlated positively with those of TNF-αa (r = 0.51 and p <0.001 vs r = 0.42 and p <0.05, respectively) and IL-1β (r = 0.52 and p <0.001 vs r = 0.49 and p <0.01, respectively), and the values of PAI-1 correlated positively with those of TNF-α (r = 0.59 and p <0.001 vs r = 0.55 and p <0.001, respectively), IL-1β (r = 0.35 and p <0.05 vs r = 0.47 and p <0.01, respectively), and TGF-β1 (r = 0.53 and p <0.001 vs r = 0.58 and p <0.001, respectively). In contrast, the levels of tPA correlated negatively with those of TNF-α (r = -0.37, p <0.05) and IL-1β (r =-0.56, p <0.001) in loculated effusions. Twenty-seven of 42 patients with loculated effusions were classified into a secondary loculation group, which, compared with the primary loculation group, had significantly higher median levels of effusion TNF-α (119.2 vs 14.2 pg/mL, respectively; p = 0.001), IL-1β (33.3 vs 3.4 pg/mL, respectively; p <0.001), TGF-β1 (13,152.7 vs 7746.0 pg/mL, respectively; p = 0.041), and PAI-1 (114.9 vs 94.1 pg/mL, respectively; p = 0.019). Conclusion: Compared with free-flowing effusions, fibrinolytic activity was depressed in loculated effusions. A higher intensity of pleural inflammation in loculated effusions may enhance the release of TNF-α, IL-1β, and TGF-β1, which may subsequently increase the levels of PAI-1. The imbalance of PAI-1 and tPA in pleural spaces may lead to fibrin deposition and loculation of pleural effusions.",
keywords = "Fibrinolysis, Loculation, Malignancy, Pleural effusion, Proinflammatory cytokines, Tuberculosis",
author = "Chung, {Chi L.} and Chen, {Chi Hung} and Sheu, {Joen Rong} and Chen, {Yi C.} and Chang, {Shi Chuan}",
year = "2005",
month = "8",
doi = "10.1378/chest.128.2.690",
language = "English",
volume = "128",
pages = "690--697",
journal = "Chest",
issn = "0012-3692",
publisher = "American College of Chest Physicians",
number = "2",

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TY - JOUR

T1 - Proinflammatory cytokines, transforming growth factor-β1, and fibrinolytic enzymes in loculated and free-flowing pleural exudates

AU - Chung, Chi L.

AU - Chen, Chi Hung

AU - Sheu, Joen Rong

AU - Chen, Yi C.

AU - Chang, Shi Chuan

PY - 2005/8

Y1 - 2005/8

N2 - Study objectives: To measure tumor necrosis factor (TNF) α, interleukin (IL) 1β, and transforming growth factor (TGF) β1 in loculated and free-flowing pleural effusions caused by malignancy, tuberculosis (TB), and pneumonia and their relationship with plasminogen activator inhibitor-type 1 (PAI-1) and tissue-type plasminogen activator (tPA) and to compare the differences between loculated and free-flowing effusions. Design: A prospective study. Patients and methods: The effusion levels of TNF-α, IL-1β, TGF-β1, PAI-1, and tPA were measured in 29 patients with malignant effusions, 19 patients with TB, and 30 patients with parapneumonic effusions. Pleural effusions were divided into loculated and free-flowing groups by imaging studies. A group of 42 patients with loculated effusions was subdivided into primary and secondary loculation groups by chest ultrasonography. Results: The median levels of TNF-α (87.0 pg/mL), IL-1β (13.8 pg/mL), TGF-β1 (10,952.9 pg/mL), PAI-1 (111.2 ng/mL), and lactate dehydrogenase (LDH) [498 IU/dL] in the loculated group were significantly higher than those in the free-flowing group (TNF-α, 15.0 pg/mL; IL-1β, 2.9 pg/mL; TGF-β1, 6,117.3 pg/mL; PAI-1, 61.5 ng/mL, and LDH, 266 IU/dL). In both the loculated and free-flowing effusions, the levels of TGF-β1 correlated positively with those of TNF-αa (r = 0.51 and p <0.001 vs r = 0.42 and p <0.05, respectively) and IL-1β (r = 0.52 and p <0.001 vs r = 0.49 and p <0.01, respectively), and the values of PAI-1 correlated positively with those of TNF-α (r = 0.59 and p <0.001 vs r = 0.55 and p <0.001, respectively), IL-1β (r = 0.35 and p <0.05 vs r = 0.47 and p <0.01, respectively), and TGF-β1 (r = 0.53 and p <0.001 vs r = 0.58 and p <0.001, respectively). In contrast, the levels of tPA correlated negatively with those of TNF-α (r = -0.37, p <0.05) and IL-1β (r =-0.56, p <0.001) in loculated effusions. Twenty-seven of 42 patients with loculated effusions were classified into a secondary loculation group, which, compared with the primary loculation group, had significantly higher median levels of effusion TNF-α (119.2 vs 14.2 pg/mL, respectively; p = 0.001), IL-1β (33.3 vs 3.4 pg/mL, respectively; p <0.001), TGF-β1 (13,152.7 vs 7746.0 pg/mL, respectively; p = 0.041), and PAI-1 (114.9 vs 94.1 pg/mL, respectively; p = 0.019). Conclusion: Compared with free-flowing effusions, fibrinolytic activity was depressed in loculated effusions. A higher intensity of pleural inflammation in loculated effusions may enhance the release of TNF-α, IL-1β, and TGF-β1, which may subsequently increase the levels of PAI-1. The imbalance of PAI-1 and tPA in pleural spaces may lead to fibrin deposition and loculation of pleural effusions.

AB - Study objectives: To measure tumor necrosis factor (TNF) α, interleukin (IL) 1β, and transforming growth factor (TGF) β1 in loculated and free-flowing pleural effusions caused by malignancy, tuberculosis (TB), and pneumonia and their relationship with plasminogen activator inhibitor-type 1 (PAI-1) and tissue-type plasminogen activator (tPA) and to compare the differences between loculated and free-flowing effusions. Design: A prospective study. Patients and methods: The effusion levels of TNF-α, IL-1β, TGF-β1, PAI-1, and tPA were measured in 29 patients with malignant effusions, 19 patients with TB, and 30 patients with parapneumonic effusions. Pleural effusions were divided into loculated and free-flowing groups by imaging studies. A group of 42 patients with loculated effusions was subdivided into primary and secondary loculation groups by chest ultrasonography. Results: The median levels of TNF-α (87.0 pg/mL), IL-1β (13.8 pg/mL), TGF-β1 (10,952.9 pg/mL), PAI-1 (111.2 ng/mL), and lactate dehydrogenase (LDH) [498 IU/dL] in the loculated group were significantly higher than those in the free-flowing group (TNF-α, 15.0 pg/mL; IL-1β, 2.9 pg/mL; TGF-β1, 6,117.3 pg/mL; PAI-1, 61.5 ng/mL, and LDH, 266 IU/dL). In both the loculated and free-flowing effusions, the levels of TGF-β1 correlated positively with those of TNF-αa (r = 0.51 and p <0.001 vs r = 0.42 and p <0.05, respectively) and IL-1β (r = 0.52 and p <0.001 vs r = 0.49 and p <0.01, respectively), and the values of PAI-1 correlated positively with those of TNF-α (r = 0.59 and p <0.001 vs r = 0.55 and p <0.001, respectively), IL-1β (r = 0.35 and p <0.05 vs r = 0.47 and p <0.01, respectively), and TGF-β1 (r = 0.53 and p <0.001 vs r = 0.58 and p <0.001, respectively). In contrast, the levels of tPA correlated negatively with those of TNF-α (r = -0.37, p <0.05) and IL-1β (r =-0.56, p <0.001) in loculated effusions. Twenty-seven of 42 patients with loculated effusions were classified into a secondary loculation group, which, compared with the primary loculation group, had significantly higher median levels of effusion TNF-α (119.2 vs 14.2 pg/mL, respectively; p = 0.001), IL-1β (33.3 vs 3.4 pg/mL, respectively; p <0.001), TGF-β1 (13,152.7 vs 7746.0 pg/mL, respectively; p = 0.041), and PAI-1 (114.9 vs 94.1 pg/mL, respectively; p = 0.019). Conclusion: Compared with free-flowing effusions, fibrinolytic activity was depressed in loculated effusions. A higher intensity of pleural inflammation in loculated effusions may enhance the release of TNF-α, IL-1β, and TGF-β1, which may subsequently increase the levels of PAI-1. The imbalance of PAI-1 and tPA in pleural spaces may lead to fibrin deposition and loculation of pleural effusions.

KW - Fibrinolysis

KW - Loculation

KW - Malignancy

KW - Pleural effusion

KW - Proinflammatory cytokines

KW - Tuberculosis

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U2 - 10.1378/chest.128.2.690

DO - 10.1378/chest.128.2.690

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