The macrophage in chronic obstructive pulmonary disease.

Macrophages are the predominant defense cell in the normal lung and during conditions associated with chronic inflammation such as COPD. However, the role of the macrophage in the development of COPD has been controversial. Scientific evidence from a variety of sources is emerging that supports a primary role for the macrophage in regulating the inflammatory response and tissue destruction associated with COPD. The role of macrophage proteinases in the development of emphysema, a major component of COPD, will be discussed. Shapiro SD. The macrophage in chronic obstructive pulmonary disease.

[1]  R. Crystal,et al.  Elastin fragments attract macrophage precursors to diseased sites in pulmonary emphysema. , 1981, Science.

[2]  T. Ley,et al.  Metalloelastase is required for macrophage-mediated proteolysis and matrix invasion in mice. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[3]  T. Ley,et al.  Molecular cloning, chromosomal localization, and bacterial expression of a murine macrophage metalloelastase. , 1992, The Journal of biological chemistry.

[4]  Shapiro Sd.  The pathogenesis of emphysema: the elastase:antielastase hypothesis 30 years later. , 1995 .

[5]  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.

[6]  E. Campbell,et al.  Quantum proteolysis resulting from release of single granules by human neutrophils: a novel, nonoxidative mechanism of extracellular proteolytic activity. , 1996, Journal of immunology.

[7]  W. Thurlbeck,et al.  Scanning electronmicroscopic morphometry of emphysema in humans. , 1994, American journal of respiratory and critical care medicine.

[8]  J. Wright.  Emphysema: concepts under change--a pathologist's perspective. , 1995, Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc.

[9]  R. Stockley,et al.  A discrete subpopulation of human monocytes expresses a neutrophil-like proinflammatory (P) phenotype. , 1994, The American journal of physiology.

[10]  S. Shapiro,et al.  Neutral proteinases of human mononuclear phagocytes. Cellular differentiation markedly alters cell phenotype for serine proteinases, metalloproteinases, and tissue inhibitor of metalloproteinases. , 1991, Journal of immunology.

[11]  T. Ley,et al.  Cloning and characterization of a unique elastolytic metalloproteinase produced by human alveolar macrophages. , 1993, The Journal of biological chemistry.

[12]  R. Mecham,et al.  Chemotactic activity of elastin-derived peptides. , 1980, The Journal of clinical investigation.

[13]  L. O’Driscoll,et al.  Matrix metalloproteinase expression and production by alveolar macrophages in emphysema. , 1997, American journal of respiratory and critical care medicine.

[14]  Z. Werb,et al.  Mouse macrophage elastase. Purification and characterization as a metalloproteinase. , 1981, The Biochemical journal.

[15]  T. Mackenzie,et al.  The human costs of tobacco use (1) , 1994, The New England journal of medicine.

[16]  S. Shapiro,et al.  Requirement for macrophage elastase for cigarette smoke-induced emphysema in mice. , 1997, Science.

[17]  Ronald McCarthy,et al.  Mice lacking neutrophil elastase reveal impaired host defense against gram negative bacterial sepsis , 1998, Nature Medicine.

[18]  L. Matrisian,et al.  The matrix metalloprotease matrilysin (PUMP) is expressed in developing human mononuclear phagocytes. , 1992, The Journal of biological chemistry.

[19]  S. Chandler,et al.  Macrophage metalloelastase degrades matrix and myelin proteins and processes a tumour necrosis factor-alpha fusion protein. , 1996, Biochemical and biophysical research communications.

[20]  Y. Okada,et al.  Collagenase expression in the lungs of transgenic mice causes pulmonary emphysema , 1992, Cell.