Lee M H, Chung S W, Kang B Y, Kim K-M, Kim T S
Department of Pharmacy and Research Institute of Drug Development, College of Pharmacy and Biotechnology Research Institute, Chonnam National University, Kwangju, Republic of Korea.
Immunology. 2002 Aug;106(4):496-502. doi: 10.1046/j.1365-2567.2002.01451.x.
Exposure to cigarette smoke is known to increase the risk of the development of allergic disease. The mechanism is not well understood. In this study, we determined the effect of hydroquinone (HQ), a major metabolite of benzene present in large quantities in cigarette tar, on interleukin-4 (IL-4) production by CD4+ T cells. HQ significantly enhanced IL-4 production by keyhole limpet haemocyanin (KLH)-primed CD4+ T cells in a dose-dependent manner. The enhancing effect of HQ on IL-4 production was maximal at a concentration of 50 micro m. It increased the level of IL-4 production approximately 10-fold. HQ enhanced IL-4 mRNA expression and also IL-4 gene promoter activity, suggesting that the enhancing effect of HQ on IL-4 production may occur at the transcriptional level. Furthermore, the injection of KLH-primed mice with HQ resulted in a significant increase in the levels of IL-4 and immunoglobulin E. These findings provide evidence that HQ, a major component of cigarette tar, may enhance allergic immune responses by inducing the production of IL-4 in CD4+ T cells.
众所周知,接触香烟烟雾会增加患过敏性疾病的风险。其机制尚不清楚。在本研究中,我们测定了对苯二酚(HQ),一种香烟焦油中大量存在的苯的主要代谢产物,对CD4 + T细胞产生白细胞介素-4(IL-4)的影响。HQ以剂量依赖的方式显著增强了由钥孔戚血蓝蛋白(KLH)致敏的CD4 + T细胞产生IL-4的能力。HQ对IL-4产生的增强作用在浓度为50微摩尔时最大。它使IL-4的产生水平增加了约10倍。HQ增强了IL-4 mRNA的表达以及IL-4基因启动子的活性,这表明HQ对IL-4产生的增强作用可能发生在转录水平。此外,给经KLH致敏的小鼠注射HQ导致IL-4和免疫球蛋白E水平显著增加。这些发现提供了证据,表明香烟焦油的主要成分HQ可能通过诱导CD4 + T细胞产生IL-4来增强过敏性免疫反应。