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The Journal of Immunology, 1999, 162: 5511-5518.
Copyright © 1999 by The American Association of Immunologists

Neutralization of the CXC Chemokine, Macrophage Inflammatory Protein-2, Attenuates Bleomycin-Induced Pulmonary Fibrosis1

Michael P. Keane*, John A. Belperio*, Thomas A. Moore*, Bethany B. Moore*, Douglas A. Arenberg*, Robert E. Smith{dagger}, Marie D. Burdick*, Steven L. Kunkel{dagger} and Robert M. Strieter2,*

* Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, and {dagger} Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109

Few studies have addressed the importance of vascular remodeling in the lung during the development of bleomycin-induced pulmonary fibrosis. For fibroplasia and deposition of extracellular matrix to occur, there must be a geometric increase in neovascularization. We hypothesized that net angiogenesis during the pathogenesis of fibroplasia and deposition of extracellular matrix during bleomycin-induced pulmonary fibrosis are dependent in part upon an overexpression of the angiogenic CXC chemokine, macrophage inflammatory protein-2 (MIP-2). To test this hypothesis, we measured MIP-2 by specific ELISA in whole lung homogenates in either bleomycin-treated or control CBA/J mice and correlated these levels with lung hydroxyproline. We found that lung tissue from mice treated with bleomycin, compared with that from saline-treated controls, demonstrated a significant increase in the presence of MIP-2 that was correlated to a greater angiogenic response and total lung hydroxyproline content. Neutralizing anti-MIP-2 Abs inhibited the angiogenic activity of day 16 bleomycin-treated lung specimens using an in vivo angiogenesis bioassay. Furthermore, when MIP-2 was depleted in vivo by passive immunization, bleomycin-induced pulmonary fibrosis was significantly reduced without a change in the presence of pulmonary neutrophils, fibroblast proliferation, or collagen gene expression. This was also paralleled by a reduction in angiogenesis. These results demonstrate that the angiogenic CXC chemokine, MIP-2, is an important factor that regulates angiogenesis/fibrosis in pulmonary fibrosis.




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