Regulation of Fas ligand expression by IL-8 in human endometrium


Selam B. , Kayisli U., Garcia-Velasco J., Akbas G., Arici A.

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, cilt.87, ss.3921-3927, 2002 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 87 Konu: 8
  • Basım Tarihi: 2002
  • Doi Numarası: 10.1210/jc.87.8.3921
  • Dergi Adı: JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
  • Sayfa Sayıları: ss.3921-3927

Özet

Numerous cytokines and growth factors are synthesized in the endometrium. IL-8 is one of these cytokines regulating endometrial function. It is a neutrophil chemoattractant/activating factor and a potent angiogenic agent. IL-8 is elevated in the peritoneal fluid of women with endometriosis. We have previously demonstrated a direct proliferative effect of IL-8 on endometrial stromal cells. We hypothesized that increased levels of IL-8 in the endometriotic environment could up-regulate Fas ligand (FasL) expression in endometrial cells and may be relevant for the development of a relative local immunotolerance in endometriosis by inducing apoptosis of cytotoxic T lymphocytes. To test our hypothesis, we studied the in vitro regulation of FasL expression and apoptosis by IL-8 in endometrial cells. Western blot analysis in endometrial stromal, glandular, and Ishikawa cells revealed that IL-8 up-regulated FasL protein expression in these cells. By semi-quantitative RT-PCR analysis, IL-8 does not alter the expression of either Fas or FasL mRNA levels in these cells. Immunocytochemistry results from endometrial stromal cells treated with IL-8 demonstrated an up-regulation of FasL protein expression. IL-8 decreased apoptosis rate in endometrial stromal cells as evaluated by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling assay. We observed an increased apoptotic rate in Jurkat (T lymphocyte line) cells plated on endometrial stromal cells previously treated with IL-8. We speculate that increased FasL expression by IL-8 may induce apoptosis of T lymphocytes and thus produce-a local immunotolerant environment for the development of ectopic implants.