Parikh A A, Moon M R, Kane C D, Salzman A L, Fischer J E, Hasselgren P O
Department of Surgery, University of Cincinnati Medical Center, Cincinnati, Ohio, 45267, USA.
J Surg Res. 1998 Jun;77(1):40-4. doi: 10.1006/jsre.1998.5332.
In recent studies, IL-1beta stimulated the production of IL-6 in human enterocytes. The heat shock response influences the production of inflammatory mediators in certain cell types. We tested the hypothesis that heat shock regulates IL-1beta-induced IL-6 production in human intestinal epithelial cells.
Cultured Caco-2 cells, a human intestinal epithelial cell line, were exposed to thermal heat shock at 43 degreesC for 1 h and recovered at 37 degreesC for 1 h. Cells were harvested for analysis of heat shock protein-70 (HSP-70) production by Western blotting. In other experiments, IL-1beta (0.5 ng/ml) was added following heat shock and recovery. IL-6 protein was measured in culture medium after 24 h by enzyme-linked immunosorbent assay and IL-6 messenger RNA (mRNA) levels were measured after 4 h by competitive reverse transcriptase polymerase chain reaction.
Heat shock resulted in the production of HSP-70 and potentiated IL-1beta-induced IL-6 production. The response to heat shock was associated with increased IL-6 mRNA levels.
The results suggest that IL-1beta-induced IL-6 production in human enterocytes is increased in association with the heat shock response. The biological role of heat shock-potentiated IL-6 production in the enterocyte remains to be determined.
在最近的研究中，白细胞介素-1β（IL-1β）刺激人肠上皮细胞产生白细胞介素-6（IL-6）。热休克反应会影响某些细胞类型中炎症介质的产生。我们检验了热休克调节人肠上皮细胞中IL-1β诱导的IL-6产生这一假说。
将人肠上皮细胞系Caco-2细胞在43℃热休克1小时，然后在37℃恢复1小时。收获细胞，通过蛋白质免疫印迹法分析热休克蛋白-70（HSP-70）的产生。在其他实验中，热休克和恢复后加入IL-1β（0.5 ng/ml）。24小时后通过酶联免疫吸附测定法测量培养基中的IL-6蛋白，4小时后通过竞争性逆转录聚合酶链反应测量IL-6信使核糖核酸（mRNA）水平。
热休克导致HSP-70产生，并增强了IL-1β诱导的IL-6产生。对热休克的反应与IL-6 mRNA水平升高有关。
结果表明，人肠上皮细胞中IL-1β诱导的IL-6产生与热休克反应相关增加。热休克增强的肠上皮细胞IL-6产生的生物学作用仍有待确定。
