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‐κB) 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‐κB 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‐κB 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‐κB pathway.