Monocyte chemotactic protein-1 concentration in peritoneal fluid of women with endometriosis and its modulation of expression in mesothelial cells.
OBJECTIVE
To investigate monocyte chemotactic protein-1 concentrations in the peritoneal fluid (PF) of women with or without endometriosis, then assess peritoneal mesothelial cells as a potential source of monocyte chemotactic protein-1.


METHODS
Prospective study.


METHODS
University medical center.


METHODS
Women with (n = 60) or without (n = 18) endometriosis.


METHODS
First monocyte chemotactic protein-1 levels in PF were measured, then mesothelial cells in culture were treated with cytokines.


METHODS
In PF and culture supernatants, monocyte chemotactic protein-1 was measured by ELISA. In vitro monocyte chemotactic protein-1 messenger RNA expression was evaluated by Northern analysis.


RESULTS
The median concentration of monocyte chemotactic protein-1 in PF of control women was 137 pg/mL (conversion factor to SI unit, 0.115; range, 12 to 418 pg/mL); that of women with moderate endometriosis was 205 pg/mL (range 65 to 6,000 pg/mL); and that of those with severe endometriosis was 1,165 pg/mL (0 to 2,602 pg/mL). Within the moderate to severe endometriosis group, monocyte chemotactic protein-1 levels were higher in women with untreated endometriosis (354 pg/mL range 0 to 6,000 pg/mL) than in women receiving GnRH agonist (128 pg/mL, range 0 to 216 pg/mL). In the control group, monocyte chemotactic protein-1 levels were higher in the proliferative phase than in the secretory phase. Mesothelial cells produced constitutively monocyte chemotactic protein-1; moreover, both interleukin-1 alpha and tumor necrosis factor-alpha induced higher levels of monocyte chemotactic protein-1.


CONCLUSIONS
Levels of monocyte chemotactic protein-1 in PF were higher during the proliferative phase than secretory phase of control women and increased in moderate to severe endometriosis. The regulated expression of monocyte chemotactic protein-1 may recruit macrophages into PF and contribute to the pathogenesis of endometriosis.
Arici
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Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut 06520-8063, USA.
Oral
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Attar
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Tazuke
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SI
Olive
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DL
D018931:Antineoplastic Agents, Hormonal / Q000627:therapeutic use; D001202:Ascitic Fluid / Q000166:cytology / Q000276:immunology*; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000032:analysis / Q000096:biosynthesis*; D004715:Endometriosis / Q000188:drug therapy / Q000276:immunology* / Q000473:pathology; D004847:Epithelial Cells; D004848:Epithelium / Q000276:immunology / Q000473:pathology; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology; D016729:Leuprolide / Q000627:therapeutic use; D008597:Menstrual Cycle; D011446:Prospective Studies; D012333:RNA, Messenger / Q000096:biosynthesis; D012016:Reference Values; D013246:Sterilization, Tubal; D014158:Transcription, Genetic; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D018931:Antineoplastic Agents, Hormonal; D018932:Chemokine CCL2; D007375:Interleukin-1; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016729:Leuprolide