Lipopolysaccharide-promoted proliferation of endometriotic stromal cells via induction of tumor necrosis factor alpha and interleukin-8 expression
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Lipopolysaccharide stimulates endometriotic stromal cell proliferation by upregulating tumor necrosis factor α and interleukin-8 expression.
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Abstract
OBJECTIVE: 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.
DESIGN: Prospective study.
SETTING: Department of Obstetrics and Gynecology, Tottori University Hospital, Yonago, Japan.
PATIENT(S): Seventeen patients who underwent laparoscopic surgery.
INTERVENTION(S): Endometriotic stromal cells were obtained from chocolate cyst linings of the ovary.
MAIN OUTCOME MEASURE(S): 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.
RESULT(S): 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.
CONCLUSION(S): Pelvic inflammation may promote the progression of endometriosis.
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- TNFalpha gene silencing reduced lipopolysaccharide-promoted proliferation of endometriotic stromal cells 2009
- A botanical extract from channel flow inhibits cell proliferation, induces apoptosis, and suppresses CCL5 in human endometriotic stromal cells 2009
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