Sharkey David J, Macpherson Anne M, Tremellen Kelton P, Robertson Sarah A
Research Centre for Reproductive Health, Discipline of Obstetrics and Gynaecology, School of Paediatrics and Reproductive Health, University of Adelaide, Adelaide SA 5005, Australia.
Mol Hum Reprod. 2007 Jul;13(7):491-501. doi: 10.1093/molehr/gam028. Epub 2007 May 5.
Exposure to semen elicits an inflammatory response in the female reproductive tract of rodents and other animals. The nature and regulation of any similar response in humans is poorly understood. This study investigated seminal plasma induction of inflammatory cytokine and chemokine gene regulation in human cervical and vaginal epithelial cells in vitro. Affymetrix microarray gene profiling revealed that inflammatory cytokine genes were prevalent among 317 known genes differentially expressed in immortalized ectocervical epithelial (Ect1) cells after incubation with pooled human seminal plasma. A dose- and time-dependent induction by seminal plasma of IL8, IL6, CSF2 and CCL2 mRNA expression in Ect1 cells was verified by quantitative RT-PCR. This was accompanied by increases in Ect1 secretion of immunoactive gene products IL-8, IL-6, GM-CSF and MCP-1. Similar cytokine responses were elicited in primary ectocervical epithelial cells. Endocervical epithelial (End1) and vaginal epithelial (Vk2) cells were less responsive to seminal fluid, with induction of IL-8 and MCP-1, but not GM-CSF or IL-6. In a panel of 10 seminal plasma samples, considerable variation in inflammatory cytokine-inducing activity was evident. These experiments show that seminal plasma can elicit expression of a range of inflammatory cytokines and chemokines in reproductive tract epithelia, and implicate the ectocervix as the primary site of responsiveness, with gene-specific differences in the kinetics and site-restrictedness of the response. Seminal factor regulation of inflammatory cytokines in the cervical epithelium is implicated in controlling the immune response to seminal antigens, and defence against infectious agents introduced at intercourse.
接触精液会在啮齿动物和其他动物的雌性生殖道中引发炎症反应。人们对人类中任何类似反应的性质和调节了解甚少。本研究在体外调查了人宫颈和阴道上皮细胞中炎性细胞因子和趋化因子基因调控的精浆诱导作用。Affymetrix微阵列基因谱分析显示,在与混合人精浆孵育后,炎性细胞因子基因在永生化宫颈外上皮(Ect1)细胞中差异表达的317个已知基因中普遍存在。通过定量RT-PCR验证了精浆对Ect1细胞中IL8、IL6、CSF2和CCL2 mRNA表达的剂量和时间依赖性诱导。这伴随着Ect1免疫活性基因产物IL-8、IL-6、GM-CSF和MCP-1分泌的增加。在原发性宫颈外上皮细胞中也引发了类似的细胞因子反应。宫颈内上皮(End1)和阴道上皮(Vk2)细胞对精液的反应较弱,仅诱导IL-8和MCP-1,而不诱导GM-CSF或IL-6。在一组10个精浆样本中,炎性细胞因子诱导活性存在明显差异。这些实验表明,精浆可在生殖道上皮细胞中引发一系列炎性细胞因子和趋化因子的表达,并表明宫颈外是主要反应部位,反应的动力学和部位限制性存在基因特异性差异。宫颈上皮中炎性细胞因子的精浆因子调节与控制对精浆抗原的免疫反应以及防御性交时引入的感染因子有关。