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<p>The human uroepithelial bladder cancer cell line T24/83 replicates <i>C. trachomatis</i> serovar D efficiently. We show here that the infection with the pathogen induces significant transcription of cytokine genes such as <i>il1β</i>, <i>il6</i> and <i>tnf</i> but not their secretion. Infected HeLa cells also do not release these cytokines with the exception of IL-6. In contrast, endotoxin, transfected polyI: C or infection with the uropathogenic <i>E. coli</i> strain CFT073 induce a robust pro-inflammatory response in T24/83 cells. These findings indicate that the cells recognize pathogen-associated molecular patterns including the TLR4 and TLR3 ligands endotoxin and dsRNA, respectively, also present in <i>C. trachomatis</i> serovar D. We, therefore, generated <i>tlr4-</i>deficient T24/83 cells to study its influence on replication of <i>C. trachomatis</i> serovar D. In contrast to our expectation, <i>C. trachomatis</i> serovar D replication in T24/83 cells did not benefit from <i>tlr4-</i>deficiency. TLR3 was reported to recognize <i>C. trachomatis</i> serovar D in the human oviduct cell line OE-E6/E7. However, <i>tlr3-</i>deficiency also did not improve the replication of the pathogen in T24/83 cells. Interestingly, <i>C. trachomatis</i> serovar D did not modulate an endotoxin-induced cytokine release but impaired significantly a polyI: C-induced and TLR3-dependent release of IFN-β. We conclude that <i>C. trachomatis</i> serovar D avoids an inflammatory reaction and circumvents recognition by TLR4 and TLR3 in infected uroepithelial T24/83 cells.</p>

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Chlamydia trachomatis serovar D replicates in uroepithelial T24/83 cells in the absence of overt inflammation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月20日

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  • Simone Albrecht,
  • Svetlana Kuhn,
  • Lina Kellner,
  • Xaver Rait,
  • Isabelle Müller,
  • Leon Heine,
  • Hannah Griffiths,
  • Carolina de la Torre,
  • Norbert Gretz,
  • Thomas Miethke

摘要

The human uroepithelial bladder cancer cell line T24/83 replicates C. trachomatis serovar D efficiently. We show here that the infection with the pathogen induces significant transcription of cytokine genes such as il1β, il6 and tnf but not their secretion. Infected HeLa cells also do not release these cytokines with the exception of IL-6. In contrast, endotoxin, transfected polyI: C or infection with the uropathogenic E. coli strain CFT073 induce a robust pro-inflammatory response in T24/83 cells. These findings indicate that the cells recognize pathogen-associated molecular patterns including the TLR4 and TLR3 ligands endotoxin and dsRNA, respectively, also present in C. trachomatis serovar D. We, therefore, generated tlr4-deficient T24/83 cells to study its influence on replication of C. trachomatis serovar D. In contrast to our expectation, C. trachomatis serovar D replication in T24/83 cells did not benefit from tlr4-deficiency. TLR3 was reported to recognize C. trachomatis serovar D in the human oviduct cell line OE-E6/E7. However, tlr3-deficiency also did not improve the replication of the pathogen in T24/83 cells. Interestingly, C. trachomatis serovar D did not modulate an endotoxin-induced cytokine release but impaired significantly a polyI: C-induced and TLR3-dependent release of IFN-β. We conclude that C. trachomatis serovar D avoids an inflammatory reaction and circumvents recognition by TLR4 and TLR3 in infected uroepithelial T24/83 cells.