Lipopolysaccharide promotes the development of murine endometriosis-like lesions via the nuclear factor-kappa B pathway

Problem: Is lipopolysaccharide (LPS) involved in the development of endometriosis? Method of Study: BALB/c mice (n=69) were used for the murine endometriosis model. Mice with surgically induced endometriosis were injected with LPS intraperitoneally. After 4 weeks of LPS injections with or without the nuclear factor-kappa B (NF-kappa B) inhibitor, the extent of endometriosis-like lesions was evaluated. Expression of inflammatory factors in the implants was evaluated using real-time RT-PCR. Cell proliferation, angiogenic activity, inflammation, and NF-kappa B phosphorylation were assessed by immunohistochemical staining. Results: Lipopolysaccharide increased total number, size, and mRNA expression of Ptgs-2, Vegf, Ccl-2, and Il-6 in endometriosis-like lesions. LPS also increased the percentage of Ki67-positive cells and enhanced the intensity and rate of positive cells of CD3, F4/80, and PECAM. Intense expression of phospho-NF-kappa B p65 after LPS administration was observed. Treatment with the NF-kB inhibitor negated these LPS-induced effects. Conclusion: LPS-induced pelvic inflammation status enhanced the development of murine endometriosis-like lesions via NF-kappa B pathway.