Tinkle S S, Schwitters P W, Newman L S
Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206, USA.
Environ Health Perspect. 1996 Oct;104 Suppl 5(Suppl 5):969-71. doi: 10.1289/ehp.96104s5969.
Chronic beryllium disease (CBD) begins as a sensitizing cell-mediated immune response to beryllium antigen that progresses to granulomatous lung disease. Previous studies demonstrated the involvement of proinflammatory cytokines in the disease process, but the pattern and regulation of cytokine release is unknown. Using bronchoalveolar lavage (BAL) cells from CBD patients in short-term tissue culture, we evaluated cytokine protein levels by enzyme-linked immunosorbent assay and T-lymphocyte proliferation by tritiated thymidine incorporation. We observed the beryllium-stimulated release of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), interleukin-2 (IL-2), and interferon-gamma (IFN-gamma) but not interleukin-4 (IL-4). Beryllium-stimulated IFN-gamma release was sustained to 168 hr in culture, whereas IL-2 concentrations returned to baseline after 24 hr. Neutralization of IL-2 decreased beryllium-stimulated T-lymphocyte proliferation, but the level of proliferation remained elevated in comparison to unstimulated BAL cells. These data suggest that T helper 1 (Th1) lymphocytes participate in the beryllium disease process; that IFN-gamma levels remain elevated after IL-2 levels return to baseline; and that IL-2 participates directly in beryllium-stimulated T-cell proliferation, but other T-lymphocyte mitogenic cytokines may be involved.
慢性铍病(CBD)始于对铍抗原的致敏性细胞介导免疫反应,该反应会发展为肉芽肿性肺病。先前的研究表明促炎细胞因子参与了疾病进程,但细胞因子释放的模式和调节尚不清楚。我们在短期组织培养中使用CBD患者的支气管肺泡灌洗(BAL)细胞,通过酶联免疫吸附测定评估细胞因子蛋白水平,并通过氚化胸腺嘧啶核苷掺入法评估T淋巴细胞增殖。我们观察到铍刺激后肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-2(IL-2)和干扰素-γ(IFN-γ)的释放,但未观察到白细胞介素-4(IL-4)的释放。铍刺激的IFN-γ释放在培养中持续至168小时,而IL-2浓度在24小时后恢复至基线。IL-2的中和降低了铍刺激的T淋巴细胞增殖,但与未刺激的BAL细胞相比,增殖水平仍升高。这些数据表明辅助性T细胞1(Th1)淋巴细胞参与了铍病进程;IL-2水平恢复至基线后IFN-γ水平仍升高;IL-2直接参与铍刺激的T细胞增殖,但可能涉及其他T淋巴细胞促有丝分裂细胞因子。