Expression of Matrix Metalloproteinase-9 in Pleural Effusions of Tuberculosis and Lung Cancer

Park, Kwang Joo; Hwang, Sung Chul; Sheen, Seung Soo; Oh, Yoon Sin; Han, Jae Ho; Lee, Kyi Beum

doi:10.1159/000084048

Cited by 42 publications

(32 citation statements)

References 65 publications

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“…MMP-9 is quantitatively the most important MMP secreted by monocytes and macrophages (Chang et al 1996; Lee et al 1999; Nagase and Woessner 1999; Kyung et al 2005;Park et al 2005), and may also be secreted by activated lymphocytes (St-Pierre et al 2003). MMP-9 secretion is of particular interest in pleural disease, since, as a gelatinase, it degrades type IV collagen and may contribute to loss of integrity of the basement membrane around blood vessels and under the mesothelial layer, leading to fluid accumulation in the pleural space (Sheen et al 2009).…”

Section: Discussionmentioning

confidence: 99%

Tissue Inhibitor of Metalloproteinase-1 Is Responsible for Residual Pleural Thickening in Pleural Tuberculosis

Hwang

Shon

Cha

et al. 2015

Tohoku J. Exp. Med.

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Residual pleural thickening (RPT) is the most frequent complication associated with pleural tuberculosis, and may occur even after successful anti-tuberculosis medications. Matrix metalloproteinases (MMPs) are zinc-dependent proteinases capable of degrading all components of the extracellular matrix. The proteolytic action of MMPs may be involved in the pathogenesis of tuberculosis. MMP-9, secreted by monocytes and lymphocyte, may lead to long-term fibrosis. The aim of the present study was to determine whether MMP-2 and/or MMP-9 and their specific inhibitors, tissue inhibitors of metalloproteinase 1 (TIMP-1) and TIMP-2, could be used to predict RPT. This retrospective study enrolled 52 patients diagnosed with pleural tuberculosis. Levels of MMP-2, MMP-9, TIMP-1, and TIM-2 were determined in the pleural fluid by ELISA. The RPT was measured on chest X-ray at the completion of treatment and the final follow-up. The average periods of anti-tuberculosis medication and the follow-up after completion of treatment were 6.7 and 7.6 months, respectively. MMP-2 or MMP-9 levels had no significant correlation to RPT. The patients with RPT > 2 mm at the completion of anti-tuberculosis medication and the final follow-up had higher TIMP-1 levels (p = 0.00 and p = 0.001, respectively). However, patients with RPT > 2 mm at the completion of anti-tuberculosis medication had lower TIMP-2 levels (p = 0.005). In a logistic regression model, elevated TIMP-1 levels at the completion of anti-tuberculosis medications were associated with RPT. In conclusion, higher TIMP-1 levels are responsible for the development of RPT and may be helpful for predicting RPT in pleural tuberculosis.

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Section: Discussionmentioning

confidence: 99%

Tissue Inhibitor of Metalloproteinase-1 Is Responsible for Residual Pleural Thickening in Pleural Tuberculosis

Hwang

Shon

Cha

et al. 2015

Tohoku J. Exp. Med.

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“…Subsequently, a number of studies focusing on specific MMPs have been reported. For example, MMP-1, -2, -8 and -9 were found to be increased in pleural fluid of patients with TB compared to patients with heart failure [21][22][23]. Circulating MMP-9 concentrations correlated with disease severity [24].…”

Section: Mmps In Tb Patients: the First Studiesmentioning

confidence: 99%

Matrix metalloproteinases in tuberculosis

Elkington¹,

Ugarte-Gil²,

Friedland³

2011

European Respiratory Journal

108

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Tuberculosis (TB) remains a global health pandemic. Infection is spread by the aerosol route and Mycobacterium tuberculosis must drive lung destruction to be transmitted to new hosts. Such inflammatory tissue damage is responsible for morbidity and mortality in patients. The underlying mechanisms of matrix destruction in TB remain poorly understood but consideration of the lung extracellular matrix predicts that matrix metalloproteinases (MMPs) will play a central role, owing to their unique ability to degrade fibrillar collagens and other matrix components. Since we proposed the concept of a matrix degrading phenotype in TB a decade ago, diverse data implicating MMPs as key mediators in TB pathology have accumulated. We review the lines of investigation that have indicated a critical role for MMPs in TB pathogenesis, consider regulatory pathways driving MMPs and propose that inhibition of MMP activity is a realistic goal as adjunctive therapy to limit immunopathology in TB.

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“…Two studies have shown upregulation of several MMPs measured by ELISA (including MMP-1, -2, -8 and -9) in tuberculous pleural fluid compared with transudates but have not related these to clinical data or correlated the MMP expression pattern with histological findings [16,17]. In a further study, PARK et al [18] demonstrated upregulated MMP-9 in tuberculous effusions compared with cancer and heart failure, but did not measure other MMPs or TIMPs that may be functionally important in the pleural space. Tuberculous pleural effusions are characterised by high monocyte and lymphocyte counts.…”

mentioning

confidence: 97%

High MMP-9 activity characterises pleural tuberculosis correlating with granuloma formation

Sheen¹,

O'Kane²,

Chaudhary³

et al. 2009

European Respiratory Journal

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Tuberculosis (TB) pleural disease is complicated by extensive tissue destruction. Matrix metalloproteinase (MMP)-1 and -9 are implicated in immunopathology of pulmonary and central nervous system TB. There are few data on MMP activity in TB pleurisy. The present study investigated MMP-1, -2 and -9 and their specific inhibitors (tissue inhibitor of metalloproteinase (TIMP)-1 and -2) in tuberculous effusions, and correlated these with clinical and histopathological features.Clinical data, routine blood tests, and pleural fluid/biopsy material were obtained from 89 patients presenting with pleural effusions in a TB-endemic area. MMP-1, -2 and -9 were measured by zymography or western blot, and TIMP-1 and -2 by ELISA. Pleural biopsies were examined microscopically, cultured for acid-alcohol fast bacilli and immunostained for MMP-9.Tuberculous pleural effusions contained the highest concentrations of MMP-9 compared with malignant effusions or heart failure transudates. MMP-9 concentrations were highest in effusions from patients with granulomatous biopsies: median (interquartile range) 108 (61-218) pg?mL -1 versus 43 (12-83) pg?mL -1 in those with nongranulomatous pleural biopsies. MMP-1 and -2 were not upregulated in tuberculous pleural fluid. The ratio of MMP-9:TIMP-1 was significantly higher in TB effusions. Tuberculous pleurisy is characterised by a specific pattern of matrix metalloproteinase-9 upregulation, correlating with the presence of granulomas and suggesting a specific role for matrix metalloproteinase-9 in inflammatory responses in tuberculous pleural disease.

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Expression of Matrix Metalloproteinase-9 in Pleural Effusions of Tuberculosis and Lung Cancer

Cited by 42 publications

References 65 publications

Tissue Inhibitor of Metalloproteinase-1 Is Responsible for Residual Pleural Thickening in Pleural Tuberculosis

Tissue Inhibitor of Metalloproteinase-1 Is Responsible for Residual Pleural Thickening in Pleural Tuberculosis

Matrix metalloproteinases in tuberculosis

High MMP-9 activity characterises pleural tuberculosis correlating with granuloma formation

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