Mio T
Chest Disease Research Institute, Kyoto University, Japan.
Nihon Kyobu Shikkan Gakkai Zasshi. 1991 Sep;29(9):1143-9.
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)
特发性肺纤维化(IPF)的一种形式,即寻常型间质性肺炎(UIP),其病理特征为在看似正常的实质组织中存在散在分布的纤维化区域。组织学显示纤维化区域有胶原蛋白和成纤维细胞过度积聚。成纤维细胞增殖通常被视为肺泡炎后的一个过程。然而,在我们的UIP病例中未观察到伴有炎症和免疫细胞增多的实质性肺泡炎。为了评估UIP中的成纤维细胞是否受正常旁分泌调节以外的机制控制,我们研究了来自UIP肺组织的肺成纤维细胞系在常规生长培养基、血小板衍生生长因子(PDGF)和前列腺素E2(PGE2)作用下的增殖特性。我们建立了10个来自IPF(UIP)患者开胸肺活检标本的成纤维细胞系和10个来自局限性肺病患者手术切除肺组织的对照成纤维细胞系。在常规生长培养基中,成纤维细胞系的倍增时间为:UIP:32.0±6.0小时(平均值±标准差),正常对照:3..2±10.4小时。两组之间无差异。为了检测PDGF的促生长活性和PGE2的生长抑制作用,将4例IPF患者的肺标本分为高强度纤维化病变组织(H)和低强度纤维化病变组织(L),并分别建立成纤维细胞系。检测有无PDGF和PGE2时的3H-胸腺嘧啶核苷摄取情况,结果以刺激指数表示。PDGF的促生长作用为:H组:1.97±1.19,L组:1.89±0.78,正常对照组:2.29±0.55。各组之间无差异。PGE2的生长抑制作用为:H组:0.88±0.24,L组:0.69±0.49,正常对照组:0.44±0.33。H组的生长抑制作用明显低于对照组(p<0.05)。L组的生长抑制作用低于对照组,但差异无统计学意义。(摘要截短至250字)