Toll-Like Receptor 4 Mediates the Response of Epithelial and Stromal Cells to Lipopolysaccharide in the Endometrium
作者： Iain Martin Sheldon , Mark H. Roberts
DOI: 10.1371/JOURNAL.PONE.0012906
关键词:
摘要: Background: Ascending infections of the female genital tract with bacteria causes pelvic inflammatory disease (PID), preterm labour and infertility. Lipopolysaccharide (LPS) is main component cell wall Gram-negative bacteria. Innate immunity relies on detection LPS by Toll-like receptor 4 (TLR4) host cells. Binding to TLR4 immune cells stimulates secretion pro-inflammatory cytokines such as IL-6, chemokines CXCL1 CCL20, prostaglandin E2. The present study tested hypothesis that endometrial epithelial stromal essential for innate response in tract. Methodology/Principal Findings: Wild type (WT) mice expressed endometrium. Intrauterine infusion purified caused disease, accumulation granulocytes throughout endometrium WT but not Tlr4 2/2 mice. Intra-peritoneal did cause PID or mice, indicating importance Stromal isolated from secreted CXCL1, CCL20 E2 LPS, a concentration time dependent manner. Co-culture combinations provided little evidence stromal-epithelial interactions LPS. Conclusions/Significance:
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