Kern J A, Lamb R J, Reed J C, Elias J A, Daniele R P
Department of Medicine, Hospital University of Pennsylvania, Philadelphia 19104-4283.
Am Rev Respir Dis. 1988 May;137(5):1180-4. doi: 10.1164/ajrccm/137.5.1180.
To assess the ability of human alveolar macrophages to produce interleukin-1-beta (IL1-beta), we examined IL1-beta mRNA accumulation in autologous monocytes and alveolar macrophages from normal volunteers. Escherichia coli lipopolysaccharide stimulation of monocytes induced rapid IL1-beta mRNA accumulation, reaching a maximum at 2 to 4 h and declining thereafter. Alveolar macrophages, however, accumulated much less mRNA than did monocytes. This difference could not be explained by differences in kinetics of IL1-beta gene expression between the 2 cell types, isolation techniques, or alveolar macrophage lidocaine exposure. This suggests that differences in transcription of the IL1-beta gene exist between these 2 cell types. Aging is a possible factor important in some functional differences between these 2 cell types. To determine if this difference in the capacity to express the IL1-beta gene might be a function of cell maturity, monocytes were aged in vitro for 7 days. After this culture period, monocytes had a marked decrease in the ability to accumulate IL1-beta mRNA, suggesting that cell aging may be one mechanism involved in producing these transcriptional differences. Because IL1-beta has also been implicated in the inflammatory and fibrotic responses in pulmonary sarcoidosis, 4 patients with newly diagnosed sarcoidosis underwent bronchoalveolar lavage, and IL1-beta mRNA accumulation was compared in their alveolar macrophages and blood monocytes. Comparing normal alveolar macrophages to those from patients with sarcoidosis showed no differences in the kinetics of IL1-beta mRNA expression or in the LPS-induced levels of IL1-beta mRNA accumulation. In addition, augmented levels of IL1-beta transcript were not noted in unstimulated sarcoid alveolar macrophages.(ABSTRACT TRUNCATED AT 250 WORDS)
为评估人类肺泡巨噬细胞产生白细胞介素-1β（IL1-β）的能力，我们检测了正常志愿者自体单核细胞和肺泡巨噬细胞中IL1-β mRNA的积累情况。用大肠杆菌脂多糖刺激单核细胞可诱导IL1-β mRNA迅速积累，在2至4小时达到峰值，随后下降。然而，肺泡巨噬细胞积累的mRNA比单核细胞少得多。这种差异无法用这两种细胞类型之间IL1-β基因表达的动力学差异、分离技术或肺泡巨噬细胞利多卡因暴露情况来解释。这表明这两种细胞类型之间存在IL1-β基因转录的差异。衰老可能是这两种细胞类型某些功能差异中的一个重要因素。为确定这种表达IL1-β基因能力的差异是否可能是细胞成熟度的函数，将单核细胞在体外培养7天。经过这段培养期后，单核细胞积累IL1-β mRNA的能力显著下降，这表明细胞衰老可能是产生这些转录差异的一种机制。由于IL1-β也与肺结节病的炎症和纤维化反应有关，对4例新诊断的结节病患者进行了支气管肺泡灌洗，并比较了他们肺泡巨噬细胞和血液单核细胞中IL1-β mRNA的积累情况。将正常肺泡巨噬细胞与结节病患者的肺泡巨噬细胞进行比较，发现IL1-β mRNA表达的动力学或脂多糖诱导的IL1-β mRNA积累水平没有差异。此外，在未刺激的结节病肺泡巨噬细胞中未观察到IL1-β转录本水平升高。（摘要截短于250字）
