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Am J Physiol Lung Cell Mol Physiol 280: L1203-L1211, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 6, L1203-L1211, June 2001

Cyclophosphamide stimulates lung fibroblasts to release neutrophil and monocyte chemoattractants

Sekiya Koyama1,2, Akemi Takamizawa2, Etsuro Sato2, Takeshi Masubuchi2, Sonoko Nagai3, and Takateru Izumi3

1 Pulmonary Section, The National Chuushin Matsumoto Hospital, Matsumoto 399-0021; 2 The First Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto 390-8621; and 3 Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto 606-8057, Japan

Cyclophosphamide is an alkylating antineoplastic agent used in several conditions. However, little is known about the mechanism of its pulmonary toxicity. In the present study, we determined that human lung fibroblasts release activity for neutrophils and monocytes in response to cyclophosphamide in a dose- and time-dependent manner. Checkerboard analysis revealed that both neutrophil and monocyte activities were chemotactic. The release of chemotactic activity was inhibited by lipoxygenase inhibitors and cycloheximide. Molecular-sieve column chromatography revealed that both neutrophil (NCA) and monocyte (MCA) chemotactic activities had multiple peaks. NCA was inhibited by a leukotriene B4 receptor antagonist and anti-interleukin-8 and anti-granulocyte colony-stimulating factor antibodies. MCA was attenuated by a leukotriene B4 receptor antagonist and anti-monocyte chemoattractant protein-1 and anti-granulocyte-macrophage colony-stimulating factor antibodies. The concentrations of interleukin-8, granulocyte colony-stimulating factor, monocyte chemoattractant protein-1, and granulocyte-macrophage colony-stimulating factor significantly increased in response to cyclophosphamide. These data suggest that lung fibroblasts may modulate inflammatory cell recruitment into the lung by releasing NCA and MCA in response to cyclophosphamide.

interstitial lung disease; interleukin-8; granulocyte colony-stimulating factor; monocyte chemoattractant protein-1; granulocyte-macrophage colony-stimulating factor


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