help button home button Am J Pathol JNCI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
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
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Huaux, F.
Right arrow Articles by Phan, S. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Huaux, F.
Right arrow Articles by Phan, S. H.
(American Journal of Pathology. 2005;167:1485-1496.)
© 2005 American Society for Investigative Pathology

Role of Eotaxin-1 (CCL11) and CC Chemokine Receptor 3 (CCR3) in Bleomycin-Induced Lung Injury and Fibrosis

Francois Huaux*{dagger}, M. Gharaee-Kermani{dagger}, Tianju Liu{dagger}, Valérie Morel{dagger}, Bridget McGarry{dagger}, Matt Ullenbruch{dagger}, Steven L. Kunkel{dagger}, Jun Wang{ddagger}, Zhou Xing{ddagger} and Sem H. Phan{dagger}

From the Unit of Industrial Toxicology and Occupational Medicine,* Université Catholique de Louvain, Brussels, Belgium; the Department of Pathology,{dagger} University of Michigan, Ann Arbor, Michigan; and the Department of Pathology,{ddagger} McMaster University, Hamilton, Canada

Eotaxin-1/CCL11 and its receptor CCR3 are involved in recruitment of eosinophils to diverse tissues, but their role in eosinophil recruitment in pulmonary fibrosis is unclear. The present study examined the pulmonary expression of CCL11 and CCR3 during bleomycin (blm)-induced lung injury and determined their importance in the recruitment of inflammatory cells and the development of lung fibrosis. In mice, blm induced a marked pulmonary expression of CCL11 and CCR3. Immunostaining for CCR3 revealed that this receptor was not only expressed by eosinophils but also by neutrophils. CCL11-deficient (CCL11–/–) mice developed significantly reduced pulmonary fibrosis. Expression of profibrotic cytokines such as transforming growth factor-ß1 was diminished in the absence of CCL11. Furthermore, increased lung expression of CCL11 significantly enhanced blm-induced lung fibrosis and production of profibrotic cytokines. These effects were also associated with an increase of eosinophil and neutrophil pulmonary infiltration. In contrast, mice treated with neutralizing CCR3 antibodies developed significantly reduced pulmonary fibrosis, eosinophilia, neutrophilia, and expression of profibrotic cytokines. Together, these data suggest that CCL11 and CCR3 are important in the pulmonary recruitment of granulocytes and play significant pathogenic roles in blm-induced lung fibrosis.




This article has been cited by other articles:


Home page
 Am. J. Respir. Crit. Care Med.Home page
I. V. Yang, L. H. Burch, M. P. Steele, J. D. Savov, J. W. Hollingsworth, E. McElvania-Tekippe, K. G. Berman, M. C. Speer, T. A. Sporn, K. K. Brown, et al.
Gene Expression Profiling of Familial and Sporadic Interstitial Pneumonia
Am. J. Respir. Crit. Care Med., January 1, 2007; 175(1): 45 - 54.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
L. A. Beck, B. Tancowny, M. E. Brummet, S. Y. Asaki, S. L. Curry, M. B. Penno, M. Foster, A. Bahl, and C. Stellato
Functional Analysis of the Chemokine Receptor CCR3 on Airway Epithelial Cells.
J. Immunol., September 1, 2006; 177(5): 3344 - 3354.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2005 by the American Society for Investigative Pathology.