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Articles in PresS, published online ahead of print February 15, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00155.2001
Submitted on May 3, 2001
Accepted on February 8, 2002
1 First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Hokkaido, Japan
2 Department of Pulmonary Medicine, Fukushima Medical University, Fukushima, Fukushima, Japan
3 Central Research Institute, Hokkaido University School of Medicine, Sapporo, Hokkaido, Japan
* To whom correspondence should be addressed. E-mail: tanino{at}sp.dianet.or.jp.
Macrophage migration inhibitory factor (MIF) is a unique cytokine which reportedly overrides the anti-inflammatory effect of endogenous glucocorticoids. MIF has been demonstrated to be involved in a variety of inflammatory diseases. In this study, we examined the role of MIF in bleomycin (BLM)-induced lung injury and fibrosis. The levels of MIF in lung tissues as well as bronchoalveolar lavage (BAL) fluids were significantly increased in the period 5 to 10 days after intratracheal administration of BLM. Treatment with the anti-MIF antibody significantly reduced the mortality at 14 days and the histopathological lung injury score at 10 days. These effects were accompanied with significant suppression of the accumulation of inflammatory cells in alveolar space and tumor necrosis factor-alpha in the lungs at 7 days. However, the anti-MIF antibody did not affect either the content of lung hydroxyproline or the histopathological lung fibrosis score at 21 days after BLM. These data provide further evidence for the crucial role of MIF in acute lung inflammation, but do not support the involvement of MIF in lung fibrosis induced by BLM in mice.
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