Hart P H, Jones C A, Jones K L, Finlay-Jones J J
Department of Microbiology & Infectious Diseases, School of Medicine, Flinders University of South Australia, Adelaide.
Immunol Cell Biol. 1993 Apr;71 ( Pt 2):99-107. doi: 10.1038/icb.1993.10.
The endogenous and lipopolysaccharide stimulated interleukin (IL)-1 beta production in vitro by peritoneal monocytes/macrophages from patients on continuous ambulatory peritoneal dialysis (CAPD) was examined during episodes of infection and inflammation. Measurement of immunoreactive IL-1 beta and bioactive IL-1 in both supernatants and cell lysates after culture for 18 h revealed that these cells secreted a significantly lower proportion of total IL-1 than that measured for elutriated blood monocytes. For the inflammatory peritoneal cells, the proportion of total IL-1 beta that was cell-associated resembled that reported for more differentiated pulmonary alveolar macrophages and for adherent monocytes cultured for 18 h prior to stimulation. A similar reduced ability to secrete IL-1 beta was detected for unfractionated peritoneal cells from CAPD patients without peritonitis upon direct comparison with the IL-1 beta production by blood mononuclear cells from the same patients. These results suggested that at a time when a pro-inflammatory response by extravasated host monocytes/macrophages was required by CAPD patients with peritonitis, only a minor proportion of total IL-1 beta would be available extracellularly. This study highlights the rapidity with which extravasated monocytes lose their ability to secrete IL-1 beta and raises the possibility that an important site of utilization of IL-1 beta in vivo may be intracellular in its location.
在感染和炎症发作期间，检测了持续性非卧床腹膜透析（CAPD）患者腹膜单核细胞/巨噬细胞在体外受内源性和脂多糖刺激产生白细胞介素（IL）-1β的情况。培养18小时后，对上清液和细胞裂解物中的免疫反应性IL-1β和生物活性IL-1进行测量，结果显示，与淘洗后的血液单核细胞相比，这些细胞分泌的总IL-1比例显著降低。对于炎性腹膜细胞，与细胞相关的总IL-1β比例与报道的更分化的肺泡巨噬细胞以及刺激前培养18小时的贴壁单核细胞相似。直接比较CAPD无腹膜炎患者未分离的腹膜细胞与同一患者血液单核细胞产生的IL-1β，发现前者分泌IL-1β的能力同样降低。这些结果表明，在腹膜炎的CAPD患者需要渗出的宿主单核细胞/巨噬细胞产生促炎反应时，细胞外可利用的总IL-1β仅占一小部分。本研究突出了渗出单核细胞丧失分泌IL-1β能力的快速性，并提出IL-1β在体内的一个重要利用部位可能在细胞内的可能性。
