Interventional Management of Pleural Infections

Heffner, John E.; Klein, Jeffrey S.; Hampson, Christopher O.

doi:10.1378/chest.08-2956

Cited by 61 publications

(45 citation statements)

References 84 publications

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“…All treatments, including uPA and PLN, induced a-SMA protein ( Figure 7A). TF expression was significantly induced by these same stimuli, with the exception of TGF-b and PLN ( Figure 7B) (2). Although PLN treatment increased TF mRNA levels, the changes were not statistically significant.…”

Section: Increased Appearance Of A-sma-expressing Pmcs In Pai-1-deficmentioning

confidence: 85%

Plasminogen Activator Inhibitor-1 Deficiency Augments Visceral Mesothelial Organization, Intrapleural Coagulation, and Lung Restriction in Mice with Carbon Black/Bleomycin–Induced Pleural Injury

Tucker¹,

Jeffers²,

Alvarez³

et al. 2014

Am J Respir Cell Mol Biol

136

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Local derangements of fibrin turnover and plasminogen activator inhibitor (PAI)-1 have been implicated in the pathogenesis of pleural injury. However, their role in the control of pleural organization has been unclear. We found that a C57Bl/6j mouse model of carbon black/bleomycin (CBB) injury demonstrates pleural organization resulting in pleural rind formation (14 d). In transgenic mice overexpressing human PAI-1, intrapleural fibrin deposition was increased, but visceral pleural thickness, lung volumes, and compliance were comparable to wild type. CBB injury in PAI-1 2/2 mice significantly increased visceral pleural thickness (P , 0.001), elastance (P , 0.05), and total lung resistance (P , 0.05), while decreasing lung compliance (P , 0.01) and lung volumes (P , 0.05). Collagen, a-smooth muscle actin, and tissue factor were increased in the thickened visceral pleura of PAI-1 2/2 mice. Colocalization of a-smooth muscle actin and calretinin within pleural mesothelial cells was increased in CBB-injured PAI-1 2/2 mice. Thrombin, factor Xa, plasmin, and urokinase induced mesothelial-mesenchymal transition, tissue factor expression, and activity in primary human pleural mesothelial cells. In PAI-1 2/2 mice, D-dimer and thrombin-antithrombin complex concentrations were increased in pleural lavage fluids. The results demonstrate that PAI-1 regulates CBB-induced pleural injury severity via unrestricted fibrinolysis and cross-talk with coagulation proteases. Whereas overexpression of PAI-1 augments intrapleural fibrin deposition, PAI-1 deficiency promotes profibrogenic alterations of the mesothelium that exacerbate pleural organization and lung restriction.

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Section: Increased Appearance Of A-sma-expressing Pmcs In Pai-1-deficmentioning

confidence: 85%

Plasminogen Activator Inhibitor-1 Deficiency Augments Visceral Mesothelial Organization, Intrapleural Coagulation, and Lung Restriction in Mice with Carbon Black/Bleomycin–Induced Pleural Injury

Tucker¹,

Jeffers²,

Alvarez³

et al. 2014

Am J Respir Cell Mol Biol

136

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“…Along these lines, PF can result from pneumonia with complicated parapneumonic pleural effusions, empyema, trauma, malignant pleural effusions that loculate, or asbestos-related pleural injury and occur in some patients that have undergone coronary artery bypass graft surgery (12,21). PF also contributes to increased mortality of patients with comorbidities including cardiac disease (4,7). Fibrosing pleuritis is characterized by infiltration of the pleural space by proliferating, ␣-smooth muscle actin (␣-SMA)-expressing myofibroblasts.…”

mentioning

confidence: 99%

Mesomesenchymal transition of pleural mesothelial cells is PI3K and NF-κB dependent

Owens

Jeffers

Boren

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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Pleural organization follows acute injury and is characterized by pleural fibrosis, which may involve the visceral and parietal pleural surfaces. This process affects patients with complicated parapneumonic pleural effusions, empyema, and other pleural diseases prone to pleural fibrosis and loculation. Pleural mesothelial cells (PMCs) undergo a process called mesothelial mesenchymal transition (MesoMT), by which PMCs acquire a profibrotic phenotype characterized by cellular enlargement and elongation, increased expression of α-smooth muscle actin (α-SMA), and matrix proteins including collagen-1. Although MesoMT contributes to pleural fibrosis and lung restriction in mice with carbon black/bleomycin-induced pleural injury and procoagulants and fibrinolytic proteases strongly induce MesoMT in vitro, the mechanism by which this transition occurs remains unclear. We found that thrombin and plasmin potently induce MesoMT in vitro as does TGF-β. Furthermore, these mediators of MesoMT activate phosphatidylinositol-3-kinase (PI3K)/Akt and NF-κB signaling pathways. Inhibition of PI3K/Akt signaling prevented TGF-β-, thrombin-, and plasmin-mediated induction of the MesoMT phenotype exhibited by primary human PMCs. Similar effects were demonstrated through blockade of the NF-κB signaling cascade using two distinctly different NF-κB inhibitors, SN50 and Bay-11 7085. Conversely, expression of constitutively active Akt-induced mesenchymal transition in human PMCs whereas the process was blocked by PX866 and AKT8. Furthermore, thrombin-mediated MesoMT is dependent on PAR-1 expression, which is linked to PI3K/Akt signaling downstream. These are the first studies to demonstrate that PI3K/Akt and/or NF-κB signaling is critical for induction of MesoMT.

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“…Evre 1 eksüdatif fazdaki sıvılar tek veya çoklu torasentez ile boşaltılabilmektedir. Ulrasonografi kılavuzluğun-da yapılan çoklu torasentezin göğüs tüpüyle aynı etkinliğe sahip olduğu gösterilmiştir (15) . Ancak tek ponksiyon ile tam olarak boşaltılamayan durumlarda çoklu ponksiyon yerine tüp torakostomi yerleştiril-mesi öncelikle önerilmektedir (7) .…”

Section: Torasentez Ile Drenajunclassified