STAT3-mediated TLR2/4 pathway upregulation in an IFN-gamma-induced Chlamydia trachomatis persistent infection model.

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.

[1]  T. Vogl,et al.  IL-6 Amplifies TLR Mediated Cytokine and Chemokine Production: Implications for the Pathogenesis of Rheumatic Inflammatory Diseases , 2014, PloS one.

[2]  D. Ojcius,et al.  Chlamydia trachomatis infection increases the expression of inflammatory tumorigenic cytokines and chemokines as well as components of the Toll-like receptor and NF-κB pathways in human prostate epithelial cells. , 2014, Molecular and cellular probes.

[3]  Yihong Yao,et al.  Targeting interleukin-6 in inflammatory autoimmune diseases and cancers. , 2014, Pharmacology & therapeutics.

[4]  B. Jenkins,et al.  Tying the knot between cytokine and toll‐like receptor signaling in gastrointestinal tract cancers , 2013, Cancer science.

[5]  H. Kita,et al.  TLR3 activation evokes IL-6 secretion, autocrine regulation of Stat3 signaling and TLR2 expression in human bronchial epithelial cells , 2013, Journal of cell communication and signaling.

[6]  A. Parker,et al.  STAT3-driven upregulation of TLR2 promotes gastric tumorigenesis independent of tumor inflammation. , 2012, Cancer cell.

[7]  S. Petrini,et al.  Amplification of the response to Toll-like receptor ligands by prolonged exposure to interleukin-6 in mice: implication for the pathogenesis of macrophage activation syndrome. , 2012, Arthritis and rheumatism.

[8]  V. Vats,et al.  Expression of TLR 2, TLR 4 and iNOS in Cervical Monocytes of Chlamydia trachomatis‐infected Women and Their Role in Host Immune Response , 2011, American journal of reproductive immunology.

[9]  G. Stark,et al.  The functions of signal transducers and activators of transcriptions 1 and 3 as cytokine-inducible proteins. , 2011, Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research.

[10]  J. Dayer,et al.  Interleukin-6: from identification of the cytokine to development of targeted treatments. , 2010, Joint, bone, spine : revue du rhumatisme.

[11]  C. Erridge.  Endogenous ligands of TLR2 and TLR4: agonists or assistants? , 2010, Journal of leukocyte biology.

[12]  R. Jha,et al.  In infertile women, cells from Chlamydia trachomatis infected site release higher levels of interferon-gamma, interleukin-10 and tumor necrosis factor-alpha upon heat shock protein stimulation than fertile women , 2008, Reproductive biology and endocrinology : RB&E.

[13]  C. Cuffini,et al.  Susceptibility of Prostate Epithelial Cells to Chlamydia muridarum Infection and Their Role in Innate Immunity by Recruitment of Intracellular Toll-Like Receptors 4 and 2 and MyD88 to the Inclusion , 2006, Infection and Immunity.

[14]  A. Visintin,et al.  Localization of TLR2 and MyD88 to Chlamydia trachomatis Inclusions , 2006, Journal of Biological Chemistry.

[15]  J. Whittimore,et al.  Chlamydia trachomatis enters a viable but non‐cultivable (persistent) state within herpes simplex virus type 2 (HSV‐2) co‐infected host cells , 2006, Cellular microbiology.

[16]  Shizuo Akira,et al.  TLR signaling pathways. , 2004, Seminars in immunology.

[17]  D. Virok,et al.  Transcriptome analysis of chlamydial growth during IFN-γ-mediated persistence and reactivation , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[18]  H. Wagner,et al.  Differential Contribution of Toll-Like Receptors 4 and 2 to the Cytokine Response to Salmonella enterica Serovar Typhimurium and Staphylococcus aureus in Mice , 2003, Infection and Immunity.

[19]  T. Darville,et al.  Differences in Innate Immune Responses (In Vitro) to HeLa Cells Infected with Nondisseminating Serovar E and Disseminating Serovar L2 of Chlamydia trachomatis , 2002, Infection and Immunity.

[20]  R. Stephens.  The cellular paradigm of chlamydial pathogenesis. , 2003, Trends in microbiology.