Selman M, Gonzalez G, Bravo M, Sullivan-Lopez J, Ramos C, Montano M, Barquin N, Vadillo F
Instituto Nacional de Enfermedades Respiratorias, Mexico, DF, Mexico.
Thorax. 1990 Jun;45(6):451-5. doi: 10.1136/thx.45.6.451.
Increased fibroblast replication and interstitial collagen accumulation occur commonly in the interstitial lung disease that progress to fibrosis. The processes controlling lung fibrogenesis are not completely understood, however. This study was designed to analyse the influence of T lymphocytes from lung tissue obtained at open lung biopsy from four patients with idiopathic pulmonary fibrosis and four patients with extrinsic allergic alveolitis on fibroblast proliferation and collagen synthesis in vitro. Lung T cell supernatants from patients with both diseases induced a moderate but significant inhibition of human lung fibroblast cell line growth. In contrast, there was a clear difference in the effect of T cells from the two groups of patients in relation to collagen production. Lung T lymphocytes from all four patients with idiopathic pulmonary fibrosis produced a substantial increase in collagen synthesis (from 371% to 514% of control values), whereas T cells from three of the four patients with extrinsic allergic alveolitis induced a significant decrease in collagen production (to 35%, 36%, and 43% of control values); in the fourth case there was an increase in collagen synthesis but this was lower than that seen with T cells from any of the patients with idiopathic pulmonary fibrosis. Peripheral T cells from six patients and control subjects caused a small increase in fibroblast proliferation and no change in collagen synthesis. The findings suggest that at least two types of interaction occur between lung T cells and fibroblasts in these disorders. A variable degree of inhibition of cell proliferation is observed in response to lung T cell supernatants from patients with both idiopathic pulmonary fibrosis and extrinsic allergic alveolitis; a substantial increase in collagen synthesis is triggered by lymphokines from patients with idiopathic pulmonary fibrosis.
在进展为纤维化的间质性肺疾病中,成纤维细胞复制增加和间质胶原积聚普遍存在。然而,控制肺纤维化形成的过程尚未完全明了。本研究旨在分析从4例特发性肺纤维化患者和4例外源性过敏性肺泡炎患者开胸肺活检获取的肺组织中的T淋巴细胞对体外成纤维细胞增殖和胶原合成的影响。两种疾病患者的肺T细胞上清液均诱导人肺成纤维细胞系生长出现中度但显著的抑制。相比之下,两组患者的T细胞在胶原产生方面的作用存在明显差异。4例特发性肺纤维化患者的肺T淋巴细胞均使胶原合成大幅增加(从对照值的371%增至514%),而4例外源性过敏性肺泡炎患者中有3例的T细胞诱导胶原产生显著减少(降至对照值的35%、36%和43%);第4例患者胶原合成增加,但低于任何特发性肺纤维化患者T细胞所观察到的增加幅度。6例患者和对照受试者的外周血T细胞使成纤维细胞增殖略有增加,胶原合成无变化。这些发现提示,在这些疾病中肺T细胞与成纤维细胞之间至少发生两种类型的相互作用。特发性肺纤维化和外源性过敏性肺泡炎患者的肺T细胞上清液均可引起不同程度的细胞增殖抑制;特发性肺纤维化患者的淋巴细胞因子可触发胶原合成大幅增加。