elastE preferred. CATHEPSIN INHIBITORS neutrophil elastase is secreted not only by proteolytic enzyme a1 antitrypsin neutrophils. The cathepsin Cyclooxygenas G a1 conjunction with AT deficiency and have asked proteinase 3 activity Th elastolytic physema suggested that endogenous inMay be inhibited with neutrophil elastase inhibitor of neutrophil elastase may be phil. Cathepsins are also released by macrophages. Tion can inactivate Re entered a1 AT, Ing uncently was found that suramin, a hex against the activity t Of neutrophil elastase and sulfonated naphthylurea cathepsins was used. Extraction of A1 from the man as anti-tumor, is a potent inhibitor of plasma is very co Expensive and a1 AT extract of cathepsin G, proteinase 3 and is used in only a few neutrophils L Direction.
This treatment must intravenously S are administered and has a half-life of only five days. This has clouded a1 to develop inhaler INHIBITORS matrixmetalloproteinases formulations.87 AT reduced matrix metalloproteinase activity T there is a group LY317615 of neutrophil elastase in patients with more than 20 closely related endopeptidases cystic fibrosis.88 However, inhaled led Inare a1 AT is capable of degrading all components of effective and co expensive and could not be Inof the extracellular re matrix of the pulmonary parenchyma, patient with severe ATdeficiency designated a1. including normal elastin, collagen, proteoglycans, recombination with subminin a1 AT Aminos acid and fibronectin. They are the institutions produced addictive Stability t may result in neutrophil alveol Be re macro but also more stable product.
Gene therapy is still phages.78 airway epithelial cells can also recover the M Possibility recently using an adenovirus vector or lipolease MMPs.79 erh Hte somes, but there were big problems in e were collagenase and gelatinase B reported a special problem with broncho gene transfer in the washing liquid a1 patients with AT deficiency emphysema.80 because large amounts of protein e bronchoalveol mu re macrophages from patients are synthesized every day. Emphysema express more gelatinase B and human a1 AT was for collagenase as cells from healthy individuals, 10 years, but also in patients with severe a1 suggesting that these cells t pleased that neutro AT deficiency and emphysema, it is that the Phils can important source of these effects MMPs.
81 marginal rate of decline FEV1.89 alveolar macrophages also express a unique There is no evidence that MMP a1 AT treatment, macrophages metalloelastase, 82, an r Key in the mouse models physema patients with normal plasma levels of play. emphysema.83 of MMP knockout M usen 12 other serine protease inhibitors do not develop emphysema and not show the example elafin can also help the Erh increase in pulmonary macrophages counexpected important for interaction elastolytic activity of t in the lungs. Elafin occurs long term exposure cigarette smoke as a specific elastase inhibitor, is in animals.84 bronchoalveol under normal tissue inhibitors of molten metal Ren lavage and is synthesized in epithelial cells loproteinases exhibitors endogenous inflammatory reaction to these m Chtigen three enzymes and stimulated Serpins .90 m may receive not be able, inhibit various