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


METHODS
Prospective study.


METHODS
Department of Obstetrics and Gynecology, Tottori University Hospital, Yonago, Japan.


METHODS
Seventeen patients who underwent laparoscopic surgery.


METHODS
Endometriotic stromal cells were obtained from chocolate cyst linings of the ovary.


METHODS
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.


RESULTS
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.


CONCLUSIONS
Pelvic inflammation may promote the progression of endometriosis.
Department of Obstetrics and Gynecology, Tottori University School of Medicine, Yonago, Japan. ibayu@grape.med.tottori-u.ac.jp
Yumiko
Y
Iba
Tasuku
T
Harada
Sayako
S
Horie
Imari
I
Deura
Tomio
T
Iwabe
Naoki
N
Terakawa
D002455:Cell Division / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004715:Endometriosis / Q000378:metabolism / Q000473:pathology*; D005260:Female; D015870:Gene Expression; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D016209:Interleukin-8 / Q000037:antagonists & inhibitors / Q000096:biosynthesis* / Q000235:genetics; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000494:pharmacology*; D008562:Membrane Glycoproteins / Q000235:genetics / Q000378:metabolism; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D016376:Oligonucleotides, Antisense / Q000494:pharmacology; D011446:Prospective Studies; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism; D013194:Staining and Labeling; D017154:Stromal Cells / Q000378:metabolism / Q000473:pathology*; D051193:Toll-Like Receptors; D014108:Tosylphenylalanyl Chloromethyl Ketone / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
D016209:Interleukin-8; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D016328:NF-kappa B; D016376:Oligonucleotides, Antisense; D011956:Receptors, Cell Surface; D051193:Toll-Like Receptors; D014409:Tumor Necrosis Factor-alpha; D014108:Tosylphenylalanyl Chloromethyl Ketone