ERJ
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Permissions
Right arrowRequest Permissions
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Iyonaga, K
Right arrow Articles by Ando, M
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Iyonaga, K
Right arrow Articles by Ando, M
Eur Respir J 1999; 14: 383-389
Copyright © ERS Journals Ltd 1999


Original Articles

Elevated bronchoalveolar concentrations of MCP-1 in patients with pulmonary alveolar proteinosis

K Iyonaga, M Suga, T Yamamoto, H Ichiyasu, H Miyakawa, and M Ando

Pulmonary alveolar proteinosis (PAP) is a rare disease of unknown aetiology characterized by accumulations of lipoproteinaceous material within the alveoli. The alveolar macrophages become increasingly foamy, and are thought to have a role in the pathogenesis of PAP. However, the mechanisms of macrophage recruitment are unclear. In the bronchoalveolar lavage fluid (BALF) of four patients with PAP and 20 normal control subjects, the following were examined: the monocyte chemotactic activity due to the chemokine monocyte chemoattractant protein (MCP)-1 with the use of a chemotactic chamber assay, the levels of MCP-1 by enzyme-linked immunosorbent assay, and the MCP-1 expression on lavage cells by immunocytochemistry and in situ hybridization. The monocyte chemotactic activity in the BALF of the PAP patients was markedly elevated, and the activity was completely absorbed by treatment with anti-MCP-1. The MCP-1 levels in the BALF were surprisingly high in the PAP group (25,100+/-472 pg x mL(-1)), whereas low levels of MCP-1 were detected in the normal control subjects (mean: never smokers 4.8; smokers 10.4 pg x mL(-1)). MCP-1 protein and messenger ribonucleic acid were expressed by macrophages from the PAP patients, and the expression was reduced according to foaming of the cells; there were monocyte-like macrophages with strong expression, small foamy cells with moderate expression, large foamy cells with a faint expression of MCP-1, and ghost cells with no expression. However, the increase of macrophage number in the PAP BALF was relatively small. These data suggest that monocyte chemoattractant protein(-1) expression by alveolar macrophages represents an amplification mechanism for the recruitment of additional macrophages to the alveoli in pulmonary alveolar proteinosis. It is possible that an ingestion of an excess of alveolar materials in pulmonary alveolar proteinosis may impair the macrophage function and the survival, resulting in the lack of a prominent increase in the macrophage number in bronchoalveolar lavage fluid.


This article has been cited by other articles:


Home page
Mayo Clin Proc.Home page
F.-C. Lin, Y.-C. Chen, and S.-C. Chang
Clinical Importance of Bronchoalveolar Lavage Fluid and Blood Cytokines, Surfactant Protein D, and Kerbs von Lungren 6 Antigen in Idiopathic Pulmonary Alveolar Proteinosis
Mayo Clin. Proc., December 1, 2008; 83(12): 1344 - 1349.
[Abstract] [Full Text] [PDF]


Home page
JEMHome page
T. Suzuki, T. Sakagami, B. K. Rubin, L. M. Nogee, R. E. Wood, S. L. Zimmerman, T. Smolarek, M. K. Dishop, S. E. Wert, J. A. Whitsett, et al.
Familial pulmonary alveolar proteinosis caused by mutations in CSF2RA
J. Exp. Med., November 24, 2008; 205(12): 2703 - 2710.
[Abstract] [Full Text] [PDF]


Home page
J. Lipid Res.Home page
M. J. Thomassen, B. P. Barna, A. G. Malur, T. L. Bonfield, C. F. Farver, A. Malur, H. Dalrymple, M. S. Kavuru, and M. Febbraio
ABCG1 is deficient in alveolar macrophages of GM-CSF knockout mice and patients with pulmonary alveolar proteinosis
J. Lipid Res., December 1, 2007; 48(12): 2762 - 2768.
[Abstract] [Full Text] [PDF]


Home page
Chronic Respiratory DiseaseHome page
O C Ioachimescu and M S Kavuru
Pulmonary alveolar proteinosis
Chronic Respiratory Disease, July 1, 2006; 3(3): 149 - 159.
[Abstract] [PDF]


Home page
J. Leukoc. Biol.Home page
T. L. Bonfield, C. M. Swaisgood, B. P. Barna, C. F. Farver, M. S. Kavuru, and M. J. Thomassen
Elevated gelatinase activity in pulmonary alveolar proteinosis: role of macrophage-colony stimulating factor
J. Leukoc. Biol., January 1, 2006; 79(1): 133 - 139.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Crit. Care Med.Home page
R. Tazawa, E. Hamano, T. Arai, H. Ohta, O. Ishimoto, K. Uchida, M. Watanabe, J. Saito, M. Takeshita, Y. Hirabayashi, et al.
Granulocyte-Macrophage Colony-Stimulating Factor and Lung Immunity in Pulmonary Alveolar Proteinosis
Am. J. Respir. Crit. Care Med., May 15, 2005; 171(10): 1142 - 1149.
[Abstract] [Full Text] [PDF]


Home page
BloodHome page
K. Uchida, K. Nakata, B. C. Trapnell, T. Terakawa, E. Hamano, A. Mikami, I. Matsushita, J. F. Seymour, M. Oh-eda, I. Ishige, et al.
High-affinity autoantibodies specifically eliminate granulocyte-macrophage colony-stimulating factor activity in the lungs of patients with idiopathic pulmonary alveolar proteinosis
Blood, February 1, 2004; 103(3): 1089 - 1098.
[Abstract] [Full Text] [PDF]


Home page
NEJMHome page
B. C. Trapnell, J. A. Whitsett, and K. Nakata
Pulmonary Alveolar Proteinosis
N. Engl. J. Med., December 25, 2003; 349(26): 2527 - 2539.
[Full Text] [PDF]


Home page
Am. J. Respir. Cell Mol. Bio.Home page
T. L. Bonfield, D. Russell, S. Burgess, A. Malur, M. S. Kavuru, and M. J. Thomassen
Autoantibodies against Granulocyte Macrophage Colony-Stimulating Factor Are Diagnostic for Pulmonary Alveolar Proteinosis
Am. J. Respir. Cell Mol. Biol., October 1, 2002; 27(4): 481 - 486.
[Abstract] [Full Text] [PDF]


Home page
Eur Respir JHome page
F. Meloni, A. Alberti, A. Bulgheroni, A. Lupi, E. Paschetto, A. Marone Bianco, G. Rodi, A. Fietta, M. Luisetti, and A. Baritussio
Surfactant apoprotein A modulates interleukin-8 and monocyte chemotactic peptide-1 production
Eur. Respir. J., June 1, 2002; 19(6): 1128 - 1135.
[Abstract] [Full Text] [PDF]


Home page
ThoraxHome page
O D Schoch, U Schanz, M Koller, K Nakata, J F Seymour, E W Russi, and A Boehler
BAL findings in a patient with pulmonary alveolar proteinosis successfully treated with GM-CSF
Thorax, March 1, 2002; 57(3): 277 - 280.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1999 by the European Respiratory Society.