McGee D W, Vitkus S J, Lee P
Department of Biological Sciences, Binghamton University (SUNY), New York 13902-6000, USA.
Cell Immunol. 1996 Mar 15;168(2):276-80. doi: 10.1006/cimm.1996.0076.
Interleukin-1 (IL-1) can induce intestinal epithelial cells (IEC) to produce several cytokines and acute phase proteins, suggesting that IEC may be important in a cytokine network at the intestinal mucosa to amplify the effects of IL-1 during an inflammatory response. However, little is known about the type of IL-1 receptor expressed by IEC and the effect of cytokines on the expression of these receptors. In this study, the expression by IEC of IL-1 receptor Type I (IL-1RI) and type II (IL-1RII) mRNA was examined by reverse transcriptase polymerase chain reaction. Both isolated rat IEC and the rat IEC-6 intestinal epithelial cell line were found to express mRNA for IL-1RI but not IL-1RII. Stimulation of the IEC-6 cells with IL-1beta or TNF-alpha down-regulated the expression of mRNA for IL-1RI at 24 hr, yet transforming growth factor-beta1 was found to have no effect. These results suggest a possible mechanism to limit the effect of IL-1 on IEC function during the mucosal inflammatory response by down-regulating the expression of the Type I IL-1 receptor.
白细胞介素-1（IL-1）可诱导肠上皮细胞（IEC）产生多种细胞因子和急性期蛋白，这表明IEC在肠道黏膜的细胞因子网络中可能起着重要作用，能够在炎症反应期间放大IL-1的效应。然而，关于IEC表达的IL-1受体类型以及细胞因子对这些受体表达的影响，人们了解甚少。在本研究中，通过逆转录聚合酶链反应检测了IEC中I型IL-1受体（IL-1RI）和II型IL-1受体（IL-1RII）mRNA的表达。结果发现，分离的大鼠IEC和大鼠IEC-6肠上皮细胞系均表达IL-1RI的mRNA，但不表达IL-1RII的mRNA。用IL-1β或TNF-α刺激IEC-6细胞24小时后，IL-1RI的mRNA表达下调，而转化生长因子-β1则无此作用。这些结果提示了一种可能的机制，即通过下调I型IL-1受体的表达来限制IL-1在黏膜炎症反应期间对IEC功能的影响。
