Problem: 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.
Results: 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.
Conclusion: Relationship between TLR4 and mPGES-1 mRNA in endometriotic lesions indicate that innate immunity may play an important role in the pathogenesis of endometriosis.
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http://dx.doi.org/10.1111/aji.12056 | DOI Listing |
Biology (Basel)
September 2024
Department of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei-shi, Tokyo 184-8588, Japan.
Toll-like receptors (TLRs) are pattern recognition receptors expressed in immune cells, including neutrophils, macrophages, and dendritic cells. Microbe-associated molecular patterns, including bacterial components, membranes, nucleic acids, and flagella are recognized by TLRs in inflammatory immune responses. Periodontal disease is an inflammatory disease known to cause local infections associated with gingival inflammation, subsequently leading to alveolar bone resorption.
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January 2023
Research Institute, NUON Co., Ltd., Seongnam 13201, Republic of Korea.
Periodontitis, a disease caused by inflammation of oral bacteria, contributes to the loss of alveolar bone and destruction of connective tissues. , a Gram-negative bacterium, is known to possess important pathogenic factors for periodontal disease. In this study, we investigated the anti-periodontitis effects of extract (MKE) and magnolin as a component of (MK) in murine macrophage RAW 264.
View Article and Find Full Text PDFNeural Regen Res
September 2021
Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu Province, China.
High mobility group box 1 (HMGB1) interacts with pattern-recognition receptors of immune cells to activate the inflammatory response. Astrocytes play a positive role in the inflammatory response of the central nervous system by expressing a broad range of pattern-recognition receptors. However, the underlying relationship between HMGB1 and the inflammatory reaction of astrocytes remains unclear.
View Article and Find Full Text PDFBiosci Trends
October 2018
Centre for Cancer and Inflammation Research, School of Chinese Medicine, Hong Kong Baptist University.
Herba Siegesbeckiae (HS, the dried aerial part of Siegesbeckia orientalis L.) is a commonly used traditional Chinese medicinal herb for treating inflammatory diseases. HS has been reported to exert anti-inflammatory effects by inhibiting the MAPKs and NF-κB pathways, the downstream effectors of TLR4 signalling.
View Article and Find Full Text PDFGlia
April 2018
Neurochemistry Research Group, Department of Psychiatry and Psychotherapy, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Hauptstr. 5, Freiburg, D-79104, Germany.
Brain inflammation is a critical factor involved in neurodegeneration. Recently, the prostaglandin E (PGE ) downstream members were suggested to modulate neuroinflammatory responses accompanying neurodegenerative diseases. In this study, we investigated the protective effects of prostaglandin E receptor 2 (EP ) during TLR3 and TLR4-driven inflammatory response using in vitro primary microglia and ex vivo organotypic hippocampal slice cultures (OHSCs).
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