title: The role of monocyte chemotactic protein-1 in intraperitoneal adhesion formation.
abstract: Abdomino-pelvic adhesions arise from infection, endometriosis, or peritoneal injury during surgery, and represent a significant source of morbidity in women of reproductive age. Monocyte chemotactic protein-1 (MCP-1) plays a role in the chemotaxis of mononuclear cells and fibroblasts in a murine wound repair model. To evaluate the role of MCP-1 in intraperitoneal adhesion formation, we investigated peritoneal fluid MCP-1 levels of women undergoing laparoscopy. Patients without endometriosis were divided into two groups: normal fertile women undergoing bilateral tubal ligation without intraperitoneal adhesions (n=14) and women with pelvic adhesions (n=8). Patients with endometriosis were arranged into two groups: women with (n=17) and without (n=17) adhesions. Peritoneal fluid MCP-1 levels were quantified using an enzyme-linked immunosorbent assay (ELISA). Peritoneal biopsy samples were immunostained for the detection of MCP-1 protein and macrophages, and were also processed for the presence of MCP-1 mRNA expression. Among women without endometriosis, the median peritoneal fluid MCP-1 level was 144 pg/ml (range 54-261) in women without adhesions and was 336 pg/ml (range 130-2494) in women with adhesions (P=0.01). There was a significant correlation between adhesion scores and MCP-1 levels (r=0.50; P=0.018). Among women with endometriosis, peritoneal fluid MCP-1 levels significantly correlated with the stage of the disease. The presence or absence of adhesions did not significantly affect the peritoneal fluid MCP-1 levels in this group of women. In summary, we have found that women with adhesions have elevated peritoneal fluid MCP-1 levels. However, we were not able to show an incremental effect of adhesions on peritoneal fluid MCP-1 levels of patients with endometriosis. Thus, we conclude that factors besides the intraperitoneal adhesions contribute to the elevated peritoneal fluid MCP-1 levels in patients with endometriosis.
authors.affiliation: Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT 06520-8063, USA.
authors.forename: H B
authors.initials: HB
authors.lastname: Zeyneloglu
authors.forename: L M
authors.initials: LM
authors.lastname: Senturk
authors.forename: E
authors.initials: E
authors.lastname: Seli
authors.forename: E
authors.initials: E
authors.lastname: Oral
authors.forename: D L
authors.initials: DL
authors.lastname: Olive
authors.forename: A
authors.initials: A
authors.lastname: Arici
mesh_terms: D000328:Adult; D000818:Animals; D001202:Ascitic Fluid / Q000378:metabolism; D001483:Base Sequence; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000235:genetics / Q000502:physiology*; D002634:Chemotaxis, Leukocyte / Q000502:physiology; D004715:Endometriosis / Q000150:complications / Q000235:genetics / Q000378:metabolism; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D051379:Mice; D015345:Oligonucleotide Probes / Q000235:genetics; D010532:Peritoneal Diseases / Q000209:etiology* / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D000267:Tissue Adhesions / Q000209:etiology / Q000235:genetics / Q000378:metabolism
chemical_list: D018932:Chemokine CCL2; D015345:Oligonucleotide Probes; D012333:RNA, Messenger