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 concentration s in the peritoneal fluid (PF) of women with or without endometriosis, then assess peritoneal mesothelial cells as a potential source of mon ocyte chemotactic protein-1. Design: Prospective study. Setting: Unive rsity medical center. Patient(s): Women with (n = 60) or without (n = 18) endometriosis. Intervention(s): First monocyte chemotactic protein -1 levels in PF were measured, then mesothelial cells in culture were treated with cytokines. Main Outcome Measure(s): In PF and culture sup ernatants, monocyte chemotactic protein-1 was measured by ELISA. In vi tro monocyte chemotactic protein-1 messenger RNA expression was evalua ted by Northern analysis. Result(s): The median concentration of monoc yte chemotactic protein-1 in PF of control women was 137 pg/mL (conver sion 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; an d 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 ch emotactic protein-1 levels were higher in women with untreated endomet riosis (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, mono cyte chemotactic protein-1 levels were higher in the proliferative pha se than in the secretory phase. Mesothelial cells produced constitutiv ely monocyte chemotactic protein-1; moreover, both interleukin-l alpha and tumor necrosis factor-alpha induced higher levels of monocyte che motactic protein-1. Conclusion(s): Levels of monocyte chemotactic prot ein-1 in PF were higher during the proliferative phase than secretory phase of control women and increased in moderate to severe endometrios is. The regulated expression of monocyte chemotactic protein-1 may rec ruit macrophages into PF and contribute to the pathogenesis of endomet riosis. (C) 1997 by American Society for Reproductive Medicine.