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Inflamm Res. 2011 Jan;60(1):69-78. doi: 10.1007/s00011-010-0237-x. Epub 2010 Aug 5.

Chlamydia trachomatis heat shock proteins 60 and 10 induce apoptosis in endocervical epithelial cells.

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1
Institute of Pathology, ICMR, Safdarjung Hospital Campus, Post Box no 4909, New Delhi 110 029, India.

Abstract

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.

PMID:
20686813
DOI:
10.1007/s00011-010-0237-x
[Indexed for MEDLINE]
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