Dysregulation of interleukin-6 responses in ectopic endometrial stromal cells: correlation with decreased soluble receptor levels in peritoneal fluid of women with endometriosis
| Autor: | Jeanne L. Becker, Sherry E. Rier, Panayota N. Zarmakoupis, Xiaoling Hu |
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| Rok vydání: | 1995 |
| Předmět: |
Adult
medicine.medical_specialty Stromal cell Adolescent Endocrinology Diabetes and Metabolism medicine.medical_treatment Clinical Biochemistry Endometriosis Uterus Biology Endometrium Biochemistry Endocrinology Internal medicine medicine Ascitic Fluid Humans Receptor Interleukin 6 Interleukin-6 Peritoneal fluid Biochemistry (medical) Receptors Interleukin medicine.disease Receptors Interleukin-6 medicine.anatomical_structure Cytokine Solubility biology.protein Female Stromal Cells |
| Zdroj: | The Journal of Clinical Endocrinology & Metabolism. 80:1431-1437 |
| ISSN: | 1945-7197 0021-972X |
| DOI: | 10.1210/jcem.80.4.7714120 |
| Popis: | Endometriosis (EM) is characterized by the aberrant growth of endometrial cells at sites outside the uterus. We showed previously that peritoneal leukocyte interleukin-6 (IL-6) production is altered in women with EM relative to that in normal control women. Because studies suggest that IL-6 may be growth regulatory for endometrial cells, we examined IL-6 and IL-6 soluble receptor (IL-6sR) in the peritoneal fluid of 40 women. In addition, the growth responsiveness of ectopic endometrial stromal cells to IL-6 was evaluated. The severity of EM correlated with increased levels of IL-6 accompanied by decreased IL-6sR in peritoneal fluid (controls, 1.0 +/- 0.1 and 525.4 +/- 53; stage I-II EM, 1.4 +/- 0.2 and 274.6 +/- 26; stage III-IV EM, 19.3 +/- 4.6 and 319.4 +/- 26; adhesions, 1.9 +/- 0.4 and 324.7 +/- 26 pmol/L IL-6 and IL-6sR, respectively). Additional studies revealed that unstimulated endometrial stromal cells from ectopic implants secreted this cytokine in vitro. Furthermore, these cells were resistant to growth inhibition induced by exposure to additional IL-6; this response correlated with weak expression of IL-6 receptor. Taken together, these findings lend further support to the hypothesis that dysregulation of IL-6 responses plays a role in the pathophysiology of EM. |
| Databáze: | OpenAIRE |
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