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      Lipopolysaccharide-promoted proliferation of endometriotic stromal cells via induction of tumor necrosis factor alpha and interleukin-8 expression.

      Fertility and Sterility
      Cell Division, drug effects, Dose-Response Relationship, Drug, Endometriosis, metabolism, pathology, Female, Gene Expression, Humans, Immunohistochemistry, methods, Interleukin-8, antagonists & inhibitors, biosynthesis, genetics, Lipopolysaccharides, administration & dosage, pharmacology, Membrane Glycoproteins, NF-kappa B, Oligonucleotides, Antisense, Prospective Studies, Receptors, Cell Surface, Staining and Labeling, Stromal Cells, Toll-Like Receptors, Tosylphenylalanyl Chloromethyl Ketone, Tumor Necrosis Factor-alpha

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          Abstract

          To evaluate the effect of lipopolysaccharide (LPS) on the expression of tumor necrosis factor alpha (TNFalpha) and interleukin-8 (IL-8) protein in endometriotic stromal cells (ESC) and their effect on the proliferation of ESC. Prospective study. Department of Obstetrics and Gynecology, Tottori University Hospital, Yonago, Japan. Seventeen patients who underwent laparoscopic surgery. Endometriotic stromal cells were obtained from chocolate cyst linings of the ovary. We determined the effect of LPS on the production of TNFalpha and IL-8 and the effect of IL-8 antisense oligonucleotide and nuclear factor-kappaB (NF-kappaB) inhibitor on IL-8 production using ELISA. TNFalpha production was examined by immunocytochemical staining. We determined the effect of LPS and the effect of IL-8 antisense oligonucleotide and NF-kappaB inhibitor on LPS-promoted ESC proliferation. LPS-stimulated ESC produced significant amounts of TNFalpha and IL-8 in a dose- and time-dependent fashion. Adding LPS promoted ESC proliferation. Anti-TNFalpha antibody and anti-IL-8 antibody inhibited the stimulatory effects of LPS. IL-8 antisense oligonucleotide and NF-kappaB inhibitor significantly decreased LPS-induced IL-8 protein production and LPS-induced ESC proliferation. Pelvic inflammation may promote the progression of endometriosis.

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