title: Interleukin-10 attenuates TNF-alpha-induced interleukin-6 production in endometriotic stromal cells.
abstract: OBJECTIVE
  To determine whether high levels of interleukin (IL)-10 can attenuate the production of tumor necrosis factor (TNF)-alpha-induced proinflammatory cytokines in endometriotic stromal cells.
  
  
  METHODS
  Prospective study.
  
  
  METHODS
  Department of Ob/Gyn, Tottori University, Japan.
  
  
  METHODS
  Thirty-five patients with ovarian endometrioma and ten patients with uterine myoma.
  
  
  METHODS
  Endometriotic stromal cells were obtained from chocolate cyst linings of ovaries. Endometrial stromal cells obtained from patient with uterine myoma.
  
  
  METHODS
  Expression of IL-10 gene in endometriotic or endometrial stromal cells was determined by real-time reverse-transcriptase polymerase chain reaction (RT-PCR). We performed immunohistochemical staining to find the presence of IL-10 and IL-10 receptors 1 and 2. We examined the effects of TNF-alpha and IL-10 on the expression of IL-6 or IL-8 by real-time RT-PCR and ELISA. We examined the activation of intracellular signal transduction molecules in endometriotic stromal cells by Western blotting.
  
  
  RESULTS
  Addition of IL-10 suppressed the expressions of IL-6 induced by TNF-alpha and IL-10 induced the phosphorylation of STAT3 in endometriotic stromal cells. TNF-alpha induced the expression of phosphorylated ERK1/2, JNK1/2, and I kappaB. Adding IL-10 suppressed the phosphorylation of these signal molecules.
  
  
  CONCLUSIONS
  Interleukin-10 attenuates TNF-alpha-induced IL-6 synthesis via NF-kappaB and MAPK pathways in endometriotic cells.. Interleukin-10 may play a significant role in the pathogenesis of endometriosis.
authors.affiliation: Department of Obstetrics and Gynecology, Tottori University School of Medicine, Yonago, Japan.
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Tagashira
authors.forename: Fuminori
authors.initials: F
authors.lastname: Taniguchi
authors.forename: Tasuku
authors.initials: T
authors.lastname: Harada
authors.forename: Ayako
authors.initials: A
authors.lastname: Ikeda
authors.forename: Ayako
authors.initials: A
authors.lastname: Watanabe
authors.forename: Naoki
authors.initials: N
authors.lastname: Terakawa
mesh_terms: D017931:DNA Primers; D004715:Endometriosis / Q000188:drug therapy / Q000473:pathology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics* / Q000378:metabolism / Q000627:therapeutic use; D015850:Interleukin-6 / Q000096:biosynthesis* / Q000235:genetics; D007889:Leiomyoma / Q000473:pathology*; D016328:NF-kappa B / Q000235:genetics; D010051:Ovarian Neoplasms / Q000473:pathology*; D012333:RNA, Messenger / Q000235:genetics; D053701:Receptors, Interleukin-10 / Q000187:drug effects / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017154:Stromal Cells / Q000187:drug effects / Q000473:pathology* / Q000502:physiology; D014157:Transcription Factors / Q000235:genetics; D014158:Transcription, Genetic; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000502:physiology*; D014594:Uterine Neoplasms / Q000473:pathology; D000093242:Interleukin-6 Inhibitors
chemical_list: D017931:DNA Primers; D016753:Interleukin-10; D015850:Interleukin-6; D016328:NF-kappa B; D012333:RNA, Messenger; D053701:Receptors, Interleukin-10; D014157:Transcription Factors; D014409:Tumor Necrosis Factor-alpha; D000093242:Interleukin-6 Inhibitors