Role of macrophage migration inhibitory factor in bleomycin-induced lung injury and fibrosis in mice

Yoshinori Tanino, Hironi Makita, Kenji Miyamoto, Tomoko Betsuyaku, Yoshinori Ohtsuka, Jun Nishihira, Masaharu Nishimura

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69 Citations (Scopus)


Macrophage migration inhibitory factor (MIF) is a unique cytokine that 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 and bronchoalveolar lavage fluids were significantly increased in the period 5-10 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 the alveolar space and tumor necrosis factor-α 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.

Original languageEnglish
Pages (from-to)L156-L162
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number1 27-1
Publication statusPublished - 2002


  • Bleomycin
  • Lung fibrosis
  • Macrophage migration inhibitory factor
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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