title: Cytokines and fibrinolytic enzymes in tuberculous and parapneumonic effusions.
abstract: Tuberculous (TB) pleurisy and parapneumonic effusion (PPE) are common causes of pleural fibrosis. The mechanisms underlying fibrin deposition may be different since involved inflammatory cells are distinct. In this study, we measured various cytokines and fibrinolytic enzymes and compared the differences between the two effusions. PPE was further divided into noncomplicated PPE and complicated PPE/empyema subgroups. Tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-8, macrophage inflammatory protein (MIP)-1beta, monocyte chemoattractant protein (MCP)-1, plasminogen activator inhibitor type 1 (PAI-1) and tissue type plasminogen activator (tPA) were measured using enzyme-linked immunosorbent assays. Significantly higher values of PAI-1, PAI-1/tPA ratio, IL-1beta, IL-8 and MIP-1beta and significantly lower values of TNF-alpha, IL-6 and MCP-1 were observed in PPE/empyema than in TB effusions. Compared to noncomplicated PPE, complicated PPE/empyema had significantly higher levels of TNF-alpha, IL-1beta, IL-8 and MIP-1beta. TB pleurisy patients who had higher effusion levels of TNF-alpha, IL-1beta and IL-8 were predisposing to residual pleural thickening. The underlying mechanisms of fibrin formation and deposition between the two effusions studied (PPE/empyema and TB pleurisy) could not be fully explained by the results of the present study. More studies are needed to explore this further.
authors.affiliation: Department of Internal Medicine, Yuan Shan Veteran Hospital, I-Lan, Taiwan.
authors.forename: Fang-Chi
authors.initials: FC
authors.lastname: Lin
authors.forename: Yi-Chu
authors.initials: YC
authors.lastname: Chen
authors.forename: Funn-Juh
authors.initials: FJ
authors.lastname: Chen
authors.forename: Shi-Chuan
authors.initials: SC
authors.lastname: Chang
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001987:Bronchiectasis / Q000097:blood / Q000378:metabolism; D018932:Chemokine CCL2 / Q000097:blood / Q000378:metabolism; D054407:Chemokine CCL4; D016207:Cytokines / Q000097:blood / Q000378:metabolism*; D016724:Empyema, Pleural / Q000097:blood / Q000378:metabolism*; D004654:Empyema, Tuberculous / Q000097:blood / Q000378:metabolism; D005260:Female; D006801:Humans; D007378:Interleukins / Q000097:blood / Q000378:metabolism; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008169:Lung Abscess / Q000097:blood / Q000378:metabolism; D019402:Macrophage Inflammatory Proteins / Q000097:blood / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood / Q000378:metabolism*; D010996:Pleural Effusion / Q000097:blood / Q000378:metabolism*; D018410:Pneumonia, Bacterial / Q000097:blood / Q000378:metabolism; D010959:Tissue Plasminogen Activator / Q000097:blood / Q000378:metabolism*; D014396:Tuberculosis, Pleural / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D054407:Chemokine CCL4; D016207:Cytokines; D007378:Interleukins; D019402:Macrophage Inflammatory Proteins; D017395:Plasminogen Activator Inhibitor 1; D014409:Tumor Necrosis Factor-alpha; D010959:Tissue Plasminogen Activator