Relationship Between Toll-like Receptor-4 and mPGES-1 Gene Expression in Local Lesions of Endometriosis Patients
Article first published online: 17 DEC 2012
© 2012 John Wiley & Sons A/S
American Journal of Reproductive Immunology
Volume 69, Issue 3, pages 231–239, March 2013
How to Cite
Relationship between Toll-like receptor-4 and mPGES-1 gene expression in local lesions of endometriosis patients. Am J Reprod Immunol 2013; 69: 231–239, , , , , , , , .
- Issue published online: 6 FEB 2013
- Article first published online: 17 DEC 2012
- Manuscript Accepted: 7 NOV 2012
- Manuscript Received: 5 SEP 2012
- microsomal prostaglandin E synthase;
- Toll-like receptor-4
Toll-like receptors (TLRs) are innate immune receptors that mediate the pattern recognition of, and response toward, pathogens and host-derived danger signals. We reported that cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase (mPGES) mRNA were expressed in cases of endometriosis. The relationship between COX-2, mPGES-1, and TLR4 in endometriotic lesions has yet to be determined.
Method of study
Endometriosis samples were obtained from 37 patients with endometrial cysts. Endometrial tissues were obtained from patients undergoing surgical procedures for benign gynecological conditions. COX-2, mPGES-1, and TLR4 mRNA expressions were examined by real-time quantitative reverse transcription PCR (qRT-PCR) and mPGES-1, and TLR4 protein localization was examined by immunohistochemistry.
TLR4 proteins were mostly located to the glandular epithelium. The immunoreactivities of TLR4 and mPGES-1 from endometriosis lesions were significantly higher than those in eutopic endometrium in the proliferative phase. The expression levels of mPGES-1 mRNA in peritoneal endometriosis were higher than those in eutopic endometrium in the proliferative phase. The expression of TLR4 mRNA correlates with that of mPGES-1 mRNA and not with that of COX-2 in endometriotic lesions.
Relationship between TLR4 and mPGES-1 mRNA in endometriotic lesions indicate that innate immunity may play an important role in the pathogenesis of endometriosis.