[Proliferative characteristics of fibroblast lines derived from open lung biopsy specimens of patients with the usual interstitial pneumonia form of idiopathic pulmonary fibrosis].
One form of idiopathic pulmonary fibrosis (IPF), usual intersitial pneumonia (UIP) is characterized pathologically by patchily distributed fibrotic areas in apparently normal parenchyma. Excessive accumulation of collagen and fibroblasts in fibrotic areas are shown histologically. Fibroblast proliferation is generally evaluated as a process following alveolitis. However, substantial alveolitis with increased inflammatory and immune cells were not observed in our UIP cases. To evaluate the possibility that fibroblasts in UIP are controlled by mechanisms other than normal paracrine regulation, proliferative features of lung fibroblast lines from UIP lung with regular growth medium, platelet derived growth factor (PDGF) and prostaglandin E2 (PGE2) were investigated. Ten fibroblast lines from open lung biopsy specimens of patients with IPF (UIP) and 10 control fibroblast lines from surgically resected lung tissues of patients with limited lung disease were established. The doubling time of fibroblast lines with regular growth medium was UIP:32.0 +/- 6.0 hrs. (mean +/- S.D.), normal control: 33.2 +/- 10.4 hrs. There was no difference between the groups. To examine growth promotion activity by PDGF and growth inhibition by PGE2, lung specimens from 4 patients with IPF were subdivided into tissue with high intensity fibrotic lesion (H) and low intensity fibrotic lesion (L), and the fibroblast lines were established separately. 3H-thymidine uptake with or without PDGF and PGE2 was examined, and results were expressed as the stimulation index. Growth promotion by PDGF was H: 1.97 +/- 1.19, L: 1.89 +/- 0.78, normal control: 2.29 +/- 0.55. There were no differences between groups. Growth inhibition by PGE2 was H: 0.88 +/- 0.24, L: 0.69 +/- 0.49, normal control: 0.44 +/- 0.33. Growth inhibition for H was significantly lower than control (p less than 0.05). Growth inhibition for L was lower than controls, but the difference was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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Chest Disease Research Institute, Kyoto University, Japan.
D000368:Aged; D002455:Cell Division; D002460:Cell Line; D015232:Dinoprostone / Q000502:physiology; D005260:Female; D005347:Fibroblasts / Q000166:cytology; D006801:Humans; D008168:Lung / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D010982:Platelet-Derived Growth Factor / Q000502:physiology; D011658:Pulmonary Fibrosis / Q000473:pathology*; D013936:Thymidine / Q000378:metabolism
D010982:Platelet-Derived Growth Factor; D015232:Dinoprostone; D013936:Thymidine