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

Abstract

Abstract 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.