| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
From the Departments of Dermatology* and Hemato-oncology and Respiratory Medicine, Kanazawa University Graduate School of Medical Science, Kanazawa, Ishikawa, Japan; and the Department of Immunology, Duke University Medical Center, Durham, North Carolina
The development of bleomycin-induced lung injury, a model of pulmonary fibrosis, results from inflammatory cell infiltration, a process highly regulated by the expression of multiple adhesion molecules. At present, the identity and role of the adhesion molecules involved in the fibrotic process are unknown. Therefore, bleomycin-induced pulmonary fibrosis was examined in mice lacking L-selectin (L-selectin-/-) expression, intercellular adhesion molecule-1 (ICAM-1) expression, or both. After 16 days of intratracheal bleomycin challenge, collagen deposition was inhibited in both L-selectin-/- and ICAM-1-/- mice when compared with wild-type littermates. Interestingly, collagen deposition was virtually eliminated in L-selectin/ICAM-1-/- mice relative to either the L-selectin-/- or ICAM-1-/- mice. Decreased pulmonary fibrosis was associated with reduced accumulation of leukocytes, including neutrophils and lymphocytes. Decreased mRNA expression of proinflammatory cytokines and transforming growth factor (TGF)-ß1 paralleled the inhibition of collagen deposition. The present study indicates that L-selectin and ICAM-1 play a critical role in pulmonary fibrosis by mediating the accumulation of leukocytes, which regulate the production of proinflammatory cytokines and TGF-ß1. This suggests that these adhesion molecules are potential therapeutic targets for inhibiting human pulmonary fibrosis.
This article has been cited by other articles:
 |
|
 |
|
  D. Voskas, Y. Babichev, L. S. Ling, J. Alami, Y. Shaked, R. S. Kerbel, B. Ciruna, and D. J. Dumont An eosinophil immune response characterizes the inflammatory skin disease observed in Tie-2 transgenic mice J. Leukoc. Biol., July 1, 2008; 84(1): 59 - 67. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Yucesoy, V. J. Johnson, G. E. Kissling, K. Fluharty, M. L. Kashon, J. Slaven, D. Germolec, V. Vallyathan, and M. I. Luster Genetic susceptibility to progressive massive fibrosis in coal miners Eur. Respir. J., June 1, 2008; 31(6): 1177 - 1182. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Horikawa, M. Fujimoto, M. Hasegawa, T. Matsushita, Y. Hamaguchi, A. Kawasuji, Y. Matsushita, T. Fujita, F. Ogawa, K. Takehara, et al. E- and P-Selectins Synergistically Inhibit Bleomycin-Induced Pulmonary Fibrosis Am. J. Pathol., September 1, 2006; 169(3): 740 - 749. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Kawasuji, M. Hasegawa, M. Horikawa, T. Fujita, Y. Matsushita, T. Matsushita, M. Fujimoto, D. A. Steeber, T. F. Tedder, K. Takehara, et al. L-selectin and intercellular adhesion molecule-1 regulate the development of Concanavalin A-induced liver injury J. Leukoc. Biol., April 1, 2006; 79(4): 696 - 705. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Murakami, N. Nagaya, T. Itoh, M. Kataoka, T. Iwase, T. Horio, Y. Miyahara, Y. Sakai, K. Kangawa, and H. Kimura Prostacyclin agonist with thromboxane synthase inhibitory activity (ONO-1301) attenuates bleomycin-induced pulmonary fibrosis in mice Am J Physiol Lung Cell Mol Physiol, January 1, 2006; 290(1): L59 - L65. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Kasper Phenotypic Characterization of Pulmonary Arteries in Normal and Diseased Lung Chest, December 1, 2005; 128(6_suppl): 547S - 552S. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Komura, M. Hasegawa, Y. Hamaguchi, E. Saito, Y. Kaburagi, K. Yanaba, S. Kawara, K. Takehara, M. Seki, D. A. Steeber, et al. Ultraviolet Light Exposure Suppresses Contact Hypersensitivity by Abrogating Endothelial Intercellular Adhesion Molecule-1 Up-Regulation at the Elicitation Site J. Immunol., September 15, 2003; 171(6): 2855 - 2862. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
