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   <subfield code="a">Chlamydia trachomatis heat shock proteins 60 and 10 induce apoptosis in endocervical epithelial cells</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Rajneesh Jha, Harsh Vardhan, Sylvette Bas, Sudha Salhan, Aruna Mittal]</subfield>
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   <subfield code="a">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 4h. 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&lt;0.05). A DNA microarray study showed significant (P&lt;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&lt;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.</subfield>
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