The regulation of lung fibroblast proliferation by alveolar macrophages--studies on the difference in the fibroblast culture conditions
Suwabe, A.; Nakamura, H.; Yakuwa, N.; Takahashi, K.; Yasui, S.
Nihon Kyobu Shikkan Gakkai Zasshi 26(6): 629-636
1988
ISSN/ISBN: 0301-1542 PMID: 3266518 Document Number: 322353
Alveolar macrophages (AM) might regulate fibroblast proliferation in the development of pulmonary fibrosis. However, results were not identical. Namely, some investigators reported that AM stimulated the lung fibroblast growth, but the others pointed to AM inhibition. In searching these conflicting results, it is important to compare the experimental results in the same conditions. There is a tendency that investigators supporting AM inhibition do the fibroblast proliferation assay under a 10% fetal calf serum (FCSZ) condition, and researchers describing the AM stimulation avoid the assays under a 10% FCS by using a platelet free plasma (PEP) or a low FCS concentration (0.4%). In this report, we recovered AM from normal rats and hamsters instilled with or without bleomycin, and prepared silica-stimulated AM culture supernatants. These supernatants stimulated the lung fibroblast growth under a 5% PEP condition, and inhibited it under a 10% FCS condition. One of the reasons about these conflicting results may be ascribed to the difference in the fibroblast culture conditions. However, the inhibition observed under a 10% FCS condition was considered to be a fibroblast "self regulation" for a "growth factor excess condition" that was caused by the addition of AM-derived growth factors (interleukin-1 or macrophage-derived growth factor (MDFG)) to a 10% FCS medium, rather than to be an AM-derived inhibition. Because; 1) the fibroblast showed the maximum growth under a 10% FCS condition, and over that concentration the fibroblast growth was inhibited, and 2) under a 10% FCS condition, even a well-known growth factor, platelet-derived growth factor (PDGF) inhibited the fibroblast proliferation without an FCS and enhance pulmonary fibrosis. It was suggested that the inhibition of the activation might be important in the therapy of pulmonary fibrosis.