STAT3-mediated TLR2/4 pathway upregulation in an IFN-gamma-induced Chlamydia trachomatis persistent infection model
STAT3-mediated TLR2/4 pathway upregulation in an IFN-gamma-induced Chlamydia trachomatis persistent infection model
复制标题
IFN-γ诱导的沙眼衣原体持续感染模型中STAT3介导的TLR2/4通路上调
DOI：
10.1093/femspd/ftw076
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发表时间：
2016
影响因子：
3.3
通讯作者：
Wang Yong
中科院分区：
文献类型：
--
作者：
Yu Ping;Xiao Lijia;Lin Lin;Tang Lingli;Chen Chunjing;Wang Fuyan;Wang Yong
沙眼衣原体引起的炎症性病理损伤，持续感染可导致多种泌尿生殖道疾病。通过比较急性和持续性c细胞模型的细胞因子产生和模式识别受体（PRR）表达。沙眼感染，我们的数据支持c。沙眼与toll样受体（TLR）2/4信号通路异常激活及IL-1α和IL-6产生升高有关，这是由信号转导和转录激活因子3 （STAT3）介导的。研究TLR信号通路异常激活对c细胞的影响。沙眼持续感染可为慢性感染治疗提供新的提示，并为了解ofC发病机制提供重要的实验基础。trachomatispersistent感染。
Inflammatory pathological injury caused byChlamydia trachomatispersistent infection could lead to a variety of urogenital tract diseases. By comparing the cytokine production and PRR (pattern recognition receptor) expression between cell models with acute or persistentC. trachomatisinfection, our data supported that persistent infection ofC. trachomatisled to abnormal activation of toll-like receptor (TLR)2/4 signaling pathway and elevated IL-1α and IL-6 production, which was mediated by signal transducer and activator of transcription3 (STAT3). Studying the effects of abnormal activation of TLR signaling pathway in the cells withC. trachomatispersistent infection could provide new hints for chronic infection treatment and an important experimental basis for understanding the pathogenesis ofC. trachomatispersistent infection.