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Updated: Jun 10, 2026

A Human Fallopian Tube Model for Investigation of C. trachomatis Infections
Published on: August 11, 2012
Chlamydia trachomatis heat shock proteins 60 and 10 induce apoptosis in endocervical epithelial cells
Rajneesh Jha1, Harsh Vardhan, Sylvette Bas
1Institute of Pathology, ICMR, Safdarjung Hospital Campus, Post Box no 4909, New Delhi 110 029, India.
Aim And Objective:
The potential role of chlamydial heat shock proteins (cHSP) 60 and cHSP10 in apoptosis of primary cervical epithelial cells was investigated.
Methods:
Primary cervical epithelial cells were stimulated with cHSP60 and cHSP10 for 4 h. Quantitative measurements of apoptosis were made using cytofluorometry, and apoptosis-related genes were analyzed by microarray, real-time PCR and western blotting. Further, levels of proinflammatory cytokines (IL-18 and IL-1β) were determined by semi-quantitative RT-PCR.
Results:
After a 4-h incubation in the presence of recombinant cHSP60 or cHSP10, the number of cells exhibiting annexin V binding activity increased 6- and 5-fold, respectively (P < 0.05). A DNA microarray study showed significant (P < 0.05) upregulation of interleukin (IL)-1 β-convertase, and caspase-3, -8 and -9 genes in cHSP60- and cHSP10-stimulated than in control cells as confirmed by real-time RT-PCR and western blotting. Transcript levels of IL-1β and IL-18 in cells treated with cHSP60 and cHSP10 were found to be significantly (P < 0.05) higher in stimulated than in control cells.
Conclusion:
cHSP60- and cHSP10-induced caspase expression, proinflammatory cytokine production and apoptosis of primary cervical epithelial cells might play a role in the pathogenesis of infertility in women with persistent chlamydial infection.
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