...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Activation of Lipid Metabolism Contributes to Interleukin-8 Production during Chlamydia trachomatis Infection of Cervical Epithelial Cells
【24h】

Activation of Lipid Metabolism Contributes to Interleukin-8 Production during Chlamydia trachomatis Infection of Cervical Epithelial Cells

机译：沙眼衣原体感染宫颈上皮细胞过程中脂质代谢的激活有助于白细胞介素8的生产。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Chlamydia trachomatis infection is the most common cause of bacterial sexually transmitted diseases. Infection of the urogenital tract by C. trachomatis causes chronic inflammation and related clinical complications. Unlike other invasive bacteria that induce a rapid cytokine/chemokine production, chlamydial infection induces delayed inflammatory response and proinflammatory chemokine production that is dependent on bacterial growth. We present data here to show that the lipid metabolism required for chlamydial growth contributes to Chlamydia-induced proinflammatory chemokine production. By gene microarray profiling, validated with biochemical studies, we found that C. trachomatis LGV2 selectively upregulated PTGS2 (COX2) and PTGER4 (EP4) in cervical epithelial HeLa 229 cells. COX2 is an enzyme that catalyzes the rate-limiting step of arachidonic acid conversion to prostaglandins, including prostaglandin E2 (PGE2) and other eicosanoids, whereas EP4 is a subtype of cell surface receptors for PGE2. We show that Chlamydia infection induced COX2 protein expression in both epithelial cells and peripheral blood mononuclear cells and promoted PGE2 release. Exogenous PGE2 was able to induce interleukin-8 release in HeLa 229 epithelial cells. Finally, we demonstrated that interleukin-8 induction by Chlamydia infection or PGE2 treatment was dependent on extracellular signal-regulated kinase/mitogen-activated protein activity. Together, these data demonstrate that the host lipid remodeling process required for chlamydial growth contributes to proinflammatory chemokine production. This study also highlights the importance of maintaining a balanced habitat for parasitic pathogens as obligate intracellular organisms.
机译：沙眼衣原体感染是细菌性传播疾病的最常见原因。 C对泌尿生殖道的感染。沙眼引起慢性炎症和相关的临床并发症。与其他诱导快速的细胞因子/趋化因子产生的侵入性细菌不同，衣原体感染诱导了延迟的炎症反应和依赖细菌生长的促炎性趋化因子的产生。我们在这里提供的数据表明，衣原体生长所需的脂质代谢有助于衣原体诱导的促炎性趋化因子产生。通过基因芯片分析，并通过生化研究验证，发现 C。沙眼LGV2选择性上调宫颈上皮HeLa 229细胞中的PTGS2（COX2）和PTGER4（EP4）。 COX2是一种催化花生四烯酸转化为前列腺素（包括前列腺素E2（PGE2）和其他类花生酸）的限速步骤的酶，而EP4是PGE2的细胞表面受体的一种亚型。我们发现衣原体感染在上皮细胞和外周血单个核细胞中均诱导了COX2蛋白的表达，并促进了PGE2的释放。外源性PGE 2能够诱导HeLa 229上皮细胞中白介素8的释放。最后，我们证明了衣原体感染或PGE2处理诱导的白细胞介素8依赖于细胞外信号调节激酶/促分裂原活化蛋白的活性。总之，这些数据表明衣原体生长所需的宿主脂质重塑过程有助于促炎性趋化因子的产生。这项研究还强调了保持寄生病原体作为专性细胞内生物的平衡栖息地的重要性。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号