Infection of human fibroblast-like synovial cells with Chlamydia trachomatis results in persistent infection and interleukin-6 production

Microb Pathog. 2003 Feb;34(2):57-63. doi: 10.1016/s0882-4010(02)00189-4.


Recent studies have shown that the urogenital pathogen Chlamydia trachomatis to be a major bacterium triggering reactive arthritis (ReA), and is able to induce interleukin-6 (IL-6) production in human fibroblast-like synovial cells (FSC) in vitro. In the present study, we examined the correlation between IL-6 production and multiplication of chlamydia in FSC. All FSC from five patients secreted highly increased quantities of IL-6 in a dose-dependent and time-dependent fashion. Heat and UV inactivated chlamydia failed to enhance production of IL-6. When azithromycin was added to infected cultures of FSC at 0 or 48 h after infection, the level of IL-6 production was very low. Transmission electron microscopy of such infected cultures revealed many abnormal forms of chlamydia within the inclusions in FSC. From one step-growth curve experiments, it was suggested that C. trachomatis hardly multiplied in FSC. In contrast, in C. trachomatis infected HeLa 229 cells, chlamydia multiplied as usual, but little IL-6 production were found. These observations indicated that live chlamydia and the persistence of chlamydia may be essential for stimulating the synthesis of IL-6 in FSC.

MeSH terms

  • Adult
  • Azithromycin / pharmacology
  • Chlamydia Infections / immunology
  • Chlamydia trachomatis / growth & development
  • Chlamydia trachomatis / physiology*
  • Chlamydia trachomatis / radiation effects
  • Chlamydia trachomatis / ultrastructure
  • Female
  • Fibroblasts / cytology
  • Fibroblasts / microbiology*
  • HeLa Cells
  • Hot Temperature
  • Humans
  • Interleukin-6 / analysis
  • Interleukin-6 / biosynthesis*
  • Male
  • Synovial Membrane / cytology
  • Synovial Membrane / immunology
  • Synovial Membrane / microbiology*
  • Ultraviolet Rays


  • Interleukin-6
  • Azithromycin