Acute cigarette smoke-induced connective tissue breakdown is mediated by neutrophils and prevented by alpha1-antitrypsin.
暂无分享,去创建一个
B. Gilks | A. Churg | R. Dhami | J. Wright | C. Xie | K. Zay | Joanne L. Wright | Blake Gilks
[1] S. Boukedes,et al. Quantum proteolysis by neutrophils : implications for pulmonary emphysema in alpha(1)-antitrypsin deficiency , 2000, Chest.
[2] M. Ko,et al. Effects of depletion of neutrophils or macrophages on development of cigarette smoke-induced emphysema. , 1999, American journal of physiology. Lung cellular and molecular physiology.
[3] J. Spinelli,et al. Z and S mutations of the alpha1-antitrypsin gene and the risk of chronic obstructive pulmonary disease. , 1999, American journal of respiratory cell and molecular biology.
[4] D. Devine,et al. Role of neutrophils and α1-antitrypsin in coal- and silica-induced connective tissue breakdown. , 1999, American journal of physiology. Lung cellular and molecular physiology.
[5] A. Lentsch,et al. Inhibition of NF-κB Activation and Augmentation of IκBβ by Secretory Leukocyte Protease Inhibitor during Lung Inflammation , 1999 .
[6] P. Smith,et al. Proton secretion in the male reproductive tract: involvement of Cl--independent[Formula: see text] transport. , 1998, American journal of physiology. Cell physiology.
[7] Y. Konttinen,et al. Matrix metalloproteinase-mediated extracellular matrix protein degradation in human pulmonary emphysema. , 1998, Laboratory investigation; a journal of technical methods and pathology.
[8] N. Anthonisen,et al. Chronic obstructive pulmonary disease (COPD). , 1998, American journal of respiratory and critical care medicine.
[9] Survival and FEV1 decline in individuals with severe deficiency of alpha1-antitrypsin. The Alpha-1-Antitrypsin Deficiency Registry Study Group. , 1998, American journal of respiratory and critical care medicine.
[10] R. Abboud,et al. Time course of neutrophil and macrophage elastinolytic activities in cigarette smoke-induced emphysema , 1998 .
[11] J. Pierce. α1-Antitrypsin Augmentation Therapy , 1997 .
[12] S. Shapiro,et al. Requirement for macrophage elastase for cigarette smoke-induced emphysema in mice. , 1997, Science.
[13] R. Abboud,et al. Effect of exposure of guinea pigs to cigarette smoke on elastolytic activity of pulmonary macrophages. , 1997, Chest.
[14] L. O’Driscoll,et al. Matrix metalloproteinase expression and production by alveolar macrophages in emphysema. , 1997, American journal of respiratory and critical care medicine.
[15] M. Selman,et al. Tobacco smoke-induced lung emphysema in guinea pigs is associated with increased interstitial collagenase. , 1996, The American journal of physiology.
[16] G. O'Connor,et al. Urinary desmosine excretion in smokers with and without rapid decline of lung function: the Normative Aging Study. , 1996, American journal of respiratory and critical care medicine.
[17] U. Kucich,et al. MR889, a neutrophil elastase inhibitor, in patients with chronic obstructive pulmonary disease: a double-blind, randomized, placebo-controlled clinical trial. , 1996, The European respiratory journal.
[18] M. Cosio,et al. Alveolar inflammation and its relation to emphysema in smokers. , 1995, American journal of respiratory and critical care medicine.
[19] D. Lomas,et al. Mutations Which Impede Loop/Sheet Polymerization Enhance the Secretion of Human α1-Antitrypsin Deficiency Variants (*) , 1995, The Journal of Biological Chemistry.
[20] G. O'Connor,et al. Elastin and collagen degradation products in urine of smokers with and without chronic obstructive pulmonary disease. , 1995, American journal of respiratory and critical care medicine.
[21] G. Snider,et al. Preliminary evidence that augmentation therapy diminishes degradation of cross-linked elastin in alpha-1-antitrypsin-deficient humans. , 1995, Respiration; international review of thoracic diseases.
[22] A. Churg,et al. Smoke-induced emphysema in guinea pigs is associated with morphometric evidence of collagen breakdown and repair. , 1995, The American journal of physiology.
[23] S. Shapiro,et al. Elastolytic metalloproteinases produced by human mononuclear phagocytes. Potential roles in destructive lung disease. , 1994, American journal of respiratory and critical care medicine.
[24] G. Snider,et al. Pitfalls in antiprotease therapy of emphysema. , 1994, American journal of respiratory and critical care medicine.
[25] H. Sekhon,et al. Cigarette smoke causes rapid cell proliferation in small airways and associated pulmonary arteries. , 1994, The American journal of physiology.
[26] M. D. de Santi,et al. Neutrophil lysosomal dysfunctions in mutant C57 Bl/6J mice: interstrain variations in content of lysosomal elastase, cathepsin G and their inhibitors. , 1994, The Biochemical journal.
[27] W. Pryor,et al. Cigarette smoking, emphysema, and damage to alpha 1-proteinase inhibitor. , 1994, The American journal of physiology.
[28] W. Thurlbeck,et al. Collagen and elastin in human pulmonary emphysema. , 1993, The American review of respiratory disease.
[29] Y. Okada,et al. Collagenase expression in the lungs of transgenic mice causes pulmonary emphysema , 1992, Cell.
[30] G. Bernard,et al. Comparison of elastin peptide concentrations in body fluids from healthy volunteers, smokers, and patients with chronic obstructive pulmonary disease. , 1992, The American review of respiratory disease.
[31] S. Shapiro,et al. Human 92- and 72-kilodalton type IV collagenases are elastases. , 1991, The Journal of biological chemistry.
[32] R. Crystal,et al. Risk factors for emphysema. Cigarette smoking is associated with a reduction in the association rate constant of lung alpha 1-antitrypsin for neutrophil elastase. , 1991, The Journal of clinical investigation.
[33] M. Cosio,et al. Cellularity of the alveolar walls in smokers and its relation to alveolar destruction. Functional implications. , 1990, The American review of respiratory disease.
[34] R. Stockley,et al. Effect of alpha-1-proteinase inhibitor on neutrophil chemotaxis. , 1990, American journal of respiratory cell and molecular biology.
[35] R. Senior,et al. Elastin degradation by human alveolar macrophages. A prominent role of metalloproteinase activity. , 1989, The American review of respiratory disease.
[36] R. Senior,et al. The inhibitory complex of human alpha 1-proteinase inhibitor and human leukocyte elastase is a neutrophil chemoattractant , 1988, The Journal of experimental medicine.
[37] R. Senior,et al. Alpha 1-proteinase inhibitor is a neutrophil chemoattractant after proteolytic inactivation by macrophage elastase. , 1988, The Journal of biological chemistry.
[38] D. Laskin,et al. Neutrophil response following intratracheal instillation of collagen peptides into rat lungs. , 1988, Experimental lung research.
[39] A. Buist,et al. Urinary excretion of desmosine (elastin cross-links) in subjects with PiZZ alpha-1-antitrypsin deficiency, a phenotype associated with hereditary predisposition to pulmonary emphysema. , 1985, The American review of respiratory disease.
[40] A Janoff,et al. Elastases and emphysema. Current assessment of the protease-antiprotease hypothesis. , 1985, The American review of respiratory disease.
[41] D. Niewoehner,et al. Cigarette smoking causes accumulation of polymorphonuclear leukocytes in alveolar septum. , 1985, The American review of respiratory disease.
[42] D. Niewoehner,et al. Urine desmosine is unrelated to cigarette smoking or to spirometric function. , 1983, The American review of respiratory disease.
[43] R. Mecham,et al. Chemotactic activity of elastin-derived peptides. , 1980, The Journal of clinical investigation.