| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Medical Research Service, Seattle Veterans Affairs Medical Center, Seattle 98108-1597; 2 Division of Pulmonary and Critical Care Medicine and 3 Division of Infectious Diseases, Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98195; and 4 Department of Immunology and Inflammation, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08540
This study investigated whether recombinant human soluble Fas ligand (rh-sFasL) induces apoptosis of primary type II pneumocytes in vitro and lung injury in vivo. Type II cells isolated from normal rabbit lung expressed Fas on their surface and became apoptotic after an 18-h incubation with rh-sFasL. Fas expression in normal rabbit lungs was localized by immunohistochemistry to alveolar and airway epithelia and alveolar macrophages. The administration of 10 µg of rh-sFasL into the right lungs of rabbits resulted 24 h later in both significantly more bronchoalveolar lavage fluid total protein and significantly more tissue changes compared with those in the left lungs, which received rh-sFasL plus Fas:Ig (a fusion protein that binds and blocks sFasL). Tissue changes included thickening of the alveolar walls, neutrophilic infiltrates, apoptotic (terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling-positive) cells in the alveolar walls, and increased expression of interleukin-8 by alveolar macrophages (as determined by immunohistochemistry). We conclude that the alveolar epithelium of normal rabbits expresses Fas and that sFasL induces lung injury and inflammation in rabbits.
pneumocytes; neutrophils; interleukin-8; macrophages
This article has been cited by other articles:
|
|
 |
|
  R. A. Bem, A. W. Farnand, V. Wong, A. Koski, M. E. Rosenfeld, N. van Rooijen, C. W. Frevert, T. R. Martin, and G. Matute-Bello Depletion of resident alveolar macrophages does not prevent Fas-mediated lung injury in mice Am J Physiol Lung Cell Mol Physiol, August 1, 2008; 295(2): L314 - L325. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. R. Martin Interactions between Mechanical and Biological Processes in Acute Lung Injury Proceedings of the ATS, April 15, 2008; 5(3): 291 - 296. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Perl, C.-S. Chung, U. Perl, J. Lomas-Neira, M. de Paepe, W. G. Cioffi, and A. Ayala Fas-induced Pulmonary Apoptosis and Inflammation during Indirect Acute Lung Injury Am. J. Respir. Crit. Care Med., September 15, 2007; 176(6): 591 - 601. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. A. Altemeier, X. Zhu, W. R. Berrington, J. M. Harlan, and W. C. Liles Fas (CD95) induces macrophage proinflammatory chemokine production via a MyD88-dependent, caspase-independent pathway J. Leukoc. Biol., September 1, 2007; 82(3): 721 - 728. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. R. Martin, N. Hagimoto, M. Nakamura, and G. Matute-Bello Apoptosis and Epithelial Injury in the Lungs Proceedings of the ATS, October 1, 2005; 2(3): 214 - 220. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. E. De Paepe, Q. Mao, Y. Chao, J. L. Powell, L. P. Rubin, and S. Sharma Hyperoxia-induced apoptosis and Fas/FasL expression in lung epithelial cells Am J Physiol Lung Cell Mol Physiol, October 1, 2005; 289(4): L647 - L659. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H Miyazaki, K Kuwano, K Yoshida, T Maeyama, M Yoshimi, M Fujita, N Hagimoto, R Yoshida, and Y Nakanishi The perforin mediated apoptotic pathway in lung injury and fibrosis J. Clin. Pathol., December 1, 2004; 57(12): 1292 - 1298. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. C. Rudkowski, E. Barreiro, R. Harfouche, P. Goldberg, O. Kishta, P. D'Orleans-Juste, J. Labonte, O. Lesur, and S. N. A. Hussain Roles of iNOS and nNOS in sepsis-induced pulmonary apoptosis Am J Physiol Lung Cell Mol Physiol, April 1, 2004; 286(4): L793 - L800. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Imai, J. Parodo, O. Kajikawa, M. de Perrot, S. Fischer, V. Edwards, E. Cutz, M. Liu, S. Keshavjee, T. R. Martin, et al. Injurious Mechanical Ventilation and End-Organ Epithelial Cell Apoptosis and Organ Dysfunction in an Experimental Model of Acute Respiratory Distress Syndrome JAMA, April 23, 2003; 289(16): 2104 - 2112. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
X. Li, H. Zhang, V. Soledad-Conrad, J. Zhuang, and B. D. Uhal Bleomycin-induced apoptosis of alveolar epithelial cells requires angiotensin synthesis de novo Am J Physiol Lung Cell Mol Physiol, March 1, 2003; 284(3): L501 - L507. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. L. Auten, M. H. Whorton, and S. Nicholas Mason Blocking Neutrophil Influx Reduces DNA Damage in Hyperoxia-Exposed Newborn Rat Lung Am. J. Respir. Cell Mol. Biol., April 1, 2002; 26(4): 391 - 397. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Matute-Bello, C. W. Frevert, W. C. Liles, M. Nakamura, J. T. Ruzinski, K. Ballman, V. A. Wong, C. Vathanaprida, and T. R. Martin Fas/Fas Ligand System Mediates Epithelial Injury, but Not Pulmonary Host Defenses, in Response to Inhaled Bacteria Infect. Immun., September 1, 2001; 69(9): 5768 - 5776. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. D. Uhal Fas and apoptosis in the alveolar epithelium: holes in the dike? Am J Physiol Lung Cell Mol Physiol, August 1, 2001; 281(2): L326 - L327. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
