fibrosis/protease

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Liver Fibrosis in HCV Monoinfected and HIV/HCV Coinfected Patients: Dysregulation of Matrix Metalloproteinases (MMPs) and Their Tissue Inhibitors TIMPs and Effect of HCV Protease Inhibitors.

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An imbalance between matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) may contribute to liver fibrosis in patients with hepatitis C (HCV) infection. We measured the circulating levels of different MMPs and TIMPs in HCV monoinfected and HIV/HCV coinfected patients

Pulmonary proteases in the cystic fibrosis lung induce interleukin 8 expression from bronchial epithelial cells via a heme/meprin/epidermal growth factor receptor/Toll-like receptor pathway.

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A high intrapulmonary protease burden is characteristic of cystic fibrosis (CF), and the resulting dysregulation of the protease/anti-protease balance has serious implications for inflammation in the CF lung. Because of this inflammation, micro-bleeds can occur releasing hemoglobin into the lung.

Clinical implication of protease-activated receptor-2 in idiopathic pulmonary fibrosis.

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Idiopathic pulmonary fibrosis (IPF) is a lethal pulmonary disease which is characterized by progressive fibrosis. In general, the exaggerated activation of the coagulation cascade has been observed during initiation or maintenance of the fibrotic disease. In a recent study, protease-activated

Role of thrombin and its major cellular receptor, protease-activated receptor-1, in pulmonary fibrosis.

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Pulmonary fibrosis is the end stage of a heterogeneous group of disorders and is characterized by the excessive deposition of extracellular matrix proteins within the pulmonary interstitium. There is increasing evidence from a number of studies that activation of the coagulation cascade, with the

Pharmacological Inhibition of Serine Proteases to Reduce Cardiac Inflammation and Fibrosis in Atrial Fibrillation.

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Systemic inflammation correlates with an increased risk of atrial fibrillation (AF) and thrombogenesis. Systemic inflammation alters vessel permeability, allowing inflammatory and immune cell migration toward target organs, including the heart. Among inflammatory cells infiltrating the atria,

Proteases of Pseudomonas aeruginosa in patients with cystic fibrosis.

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Radioimmunoassays were used to determine titers of antibody to alkaline protease (AP) and elastase (Ela) produced by Pseudomonas aeruginosa in sera and bronchial secretions, in vitro production of AP and Ela by P. aeruginosa isolates, and occurrence of these enzymes in bronchial secretions from

Production of elastase, exotoxin A, and alkaline protease in sputa during pulmonary exacerbation of cystic fibrosis in patients chronically infected by Pseudomonas aeruginosa.

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Secretion of Pseudomonas aeruginosa elastase, exotoxin A, and alkaline protease in sputum during bronchopulmonary exacerbations was examined in 18 cystic fibrosis patients chronically infected with this microorganism. The patients were studied during one or several exacerbation periods necessitating

Detection of proteases of Pseudomonas aeruginosa in immune complexes isolated from sputum of cystic fibrosis patients.

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Sera and sputa of 12 cystic fibrosis patients suffering from chronic Pseudomonas aeruginosa lung infections were assayed for immune complexes using the Raji cell assay. Whereas all sera were negative, 33% of the sputa were positive for immune complexes. Sera and sputa of these patients were also

Cystic fibrosis: protease activity in saliva evaluated with chromogenic substrates.

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The protease activities in saliva from individuals with cystic fibrosis (CF) were studied using four different chromogenic substrates. In the CF-group a significantly decreased protease activity in the range 50-70% was found, compared to an age- and sex-matched control group, but with considerable

Secretory leukocyte protease inhibitor in cystic fibrosis.

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Cystic fibrosis (CF) is a genetic disorder that leads to a defect in chloride ion transport and results in pancreatic and pulmonary insufficiency. The pulmonary disease is characterized by bacterial colonization and inflammation with excessive levels of neutrophils and neutrophil elastase within the

Cystic fibrosis sputum induces a secretory response from airway gland serous cells that can be prevented by neutrophil protease inhibitors.

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High activities of the neutrophil proteases, elastase and cathepsin G, are found in the sputum of patients with cystic fibrosis (CF). Because both proteases have been shown to be potent secretagogues for airway submucosal glands, and because hypersecretion is a characteristic feature of CF, the

Decreased activity of hepatic alkaline protease in rats with carbon tetrachloride-induced liver cirrhosis.

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To investigate the cause of accumulation of oxidised proteins in the livers of rats with carbon tetrachloride (CCl4) induced liver cirrhosis, the activity of alkaline protease (a high molecular weight, multisubunit cysteine proteinase) was determined in the cirrhotic livers. A significant decrease

Human airway trypsin-like protease exerts potent, antifibrotic action in pulmonary fibrosis.

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Idiopathic pulmonary fibrosis (IPF) is characterized by the deposition of excessive extracellular matrix and the destruction of lung parenchyma, resulting from an aberrant wound-healing response. Although IPF is often associated with an imbalance in protease activity, the mechanisms underlying the

Persistent Salmonella enterica Serovar Typhimurium Infection Induces Protease Expression During Intestinal Fibrosis.

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Intestinal fibrosis is a common and serious complication of Crohn's disease characterized by the accumulation of fibroblasts, deposition of extracellular matrix, and formation of scar tissue. Although many factors including cytokines and proteases contribute to the development of

Reaction of 4-methylumbelliferylguanidinobenzoate with proteases in plasma of patients with cystic fibrosis.

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Protease activity, assayed using 4-methylumbelliferylguanidinobenzoate, an active site titrant of certain proteases, is significantly deficient in plasma of patients with cystic fibrosis. The deficiency can be demonstrated with both chloroform-ellagic acid activated plasma in which the proteases can

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