Conclusion
Lipopolysaccharide exposure disrupted implantation and decidualization in mice and human endometrial stromal cells. This model could be used to study the pathophysiology of implantation failure in patients with chronic endometritis or to test potential therapeutic interventions.
Results
Lipopolysaccharide treatment resulted in fewer implantation sites in mice, decreased expression of decidualization-associated genes, and altered expression and release of cytokines and chemokines. Immunohistological analysis of the uterus from LPS-exposed mice demonstrated increased apoptosis and decreased proliferation during decidualization.