title: STAT3-mediated TLR2/4 pathway upregulation in an IFN-gamma-induced Chlamydia trachomatis persistent infection model.
abstract: Inflammatory pathological injury caused by Chlamydia trachomatis persistent 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 persistent C. trachomatis infection, our data supported that persistent infection of C. trachomatis led 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 with C. trachomatis persistent infection could provide new hints for chronic infection treatment and an important experimental basis for understanding the pathogenesis of C. trachomatis persistent infection.
authors: Department of Immunology, School of Basic Medical Science, Xiangya School of Medicine, Central South University, Changsha, Hunan 410013, China.
authors: Ping
authors: P
authors: Yu
authors: Department of Immunology, School of Basic Medical Science, Xiangya School of Medicine, Central South University, Changsha, Hunan 410013, China.
authors: Lijia
authors: L
authors: Xiao
authors: Department of Immunology, School of Basic Medical Science, Xiangya School of Medicine, Central South University, Changsha, Hunan 410013, China.
authors: Lin
authors: L
authors: Lin
authors: Clinical Laboratory, The Second Xiangya Hospital of Central South University, Central South University, Renminzhong Road 139, Changsha, Hunan 410011, China.
authors: Lingli
authors: L
authors: Tang
authors: Department of Immunology, School of Basic Medical Science, Xiangya School of Medicine, Central South University, Changsha, Hunan 410013, China.
authors: Chunjing
authors: C
authors: Chen
authors: Department of Immunology, School of Basic Medical Science, Xiangya School of Medicine, Central South University, Changsha, Hunan 410013, China.
authors: Fuyan
authors: F
authors: Wang
authors: Department of Immunology, School of Basic Medical Science, Xiangya School of Medicine, Central South University, Changsha, Hunan 410013, China wangyong@csu.edu.cn.
authors: Yong
authors: Y
authors: Wang
mesh_terms: D000208:Acute Disease; D002478:Cells, Cultured; D002690:Chlamydia Infections / Q000235:genetics / Q000378:metabolism / Q000382:microbiology; D002692:Chlamydia trachomatis / Q000502:physiology*; D002908:Chronic Disease; D016207:Cytokines / Q000378:metabolism; D020869:Gene Expression Profiling; D020868:Gene Silencing; D006367:HeLa Cells; D054884:Host-Pathogen Interactions; D006801:Humans; D066298:In Vitro Techniques; D018836:Inflammation Mediators / Q000378:metabolism; D007371:Interferon-gamma / Q000378:metabolism*; D050796:STAT3 Transcription Factor / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction; D051195:Toll-Like Receptor 2 / Q000378:metabolism*; D051197:Toll-Like Receptor 4 / Q000378:metabolism*; D059467:Transcriptome
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D050796:STAT3 Transcription Factor; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D007371:Interferon-gamma
keywords: PRR; chronic inflammation; host–pathogen interaction; inflammatory cytokine