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Am J Physiol Lung Cell Mol Physiol 275: L687-L693, 1998;
1040-0605/98 $5.00
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Vol. 275, Issue 4, L687-L693, October 1998

Alveolar type II-like cells release G-CSF as neutrophil chemotactic activity

Sekiya Koyama1,2, Etsuro Sato1, Takeshi Masubuchi1, Akemi Takamizawa1, Keishi Kubo1, Sonoko Nagai2, and Takateru Izumi2

1 The First Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto 390; and 2 Chest Disease Research Institute, Kyoto University, Sakyoku, Kyoto 606-01, Japan

We evaluated the potential of A549 cells, an alveolar type II epithelial cell line, to release granulocyte colony-stimulating factor (G-CSF), in addition to interleukin (IL)-8 and leukotriene B4, as neutrophil chemotactic activity (NCA). Human recombinant IL-1beta stimulated A549 cells to release NCA in a time- and dose-dependent fashion. The released NCA was blocked by mouse anti-human G-CSF polyclonal antibody. Molecular-sieve column chromatography revealed that IL-1beta induced the release of a 19- to 20-kDa chemotactic mass that was inhibited by anti-human G-CSF antibody. IL-1beta stimulated the release of G-CSF in a dose-dependent fashion, but the time-dependent profile of G-CSF showed that the concentration of G-CSF declined after 48 h. Tumor necrosis factor (TNF)-alpha , Escherichia coli lipopolysaccharide (LPS), and bradykinin (BK) stimulated A549 cells to release NCA that was inhibited by anti-G-CSF antibody. The release of G-CSF in response to TNF-alpha , LPS, and BK was significantly increased. The similar concentrations of human recombinant G-CSF (10-1,000 pg/ml) as in the supernatant fluid induced neutrophil chemotaxis. G-CSF mRNA was expressed time and dose dependently at 4 h and declined after 4 h in response to IL-1beta as evaluated by RT-PCR. The expression of G-CSF mRNA was also observed by TNF-alpha , LPS, and BK stimulation. These data suggest that type II alveolar epithelial cells may produce G-CSF as NCA and may participate in the regulation of leukocyte extravasation.

granulocyte colony-stimulating factor; type II pneumocyte; neutrophil chemotaxis


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