The Role of Monocyte Chemotactic Protein-1 in Intraperitoneal Adhesion Formation*

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.

[1]  A. Arıcı,et al.  The effect of monocyte chemotactic protein 1 in intraperitoneal adhesion formation in a mouse model. , 1998, American journal of obstetrics and gynecology.

[2]  S. Tazuke,et al.  Monocyte chemotactic protein-1 concentration in peritoneal fluid of women with endometriosis and its modulation of expression in mesothelial cells. , 1997, Fertility and sterility.

[3]  R. Kelly,et al.  Chemokine and cyclooxygenase-2 expression in human endometrium coincides with leukocyte accumulation. , 1997, Human reproduction.

[4]  D. Charnock-Jones,et al.  Decreased levels of the potent regulator of monocyte/macrophage activation, interleukin-13, in the peritoneal fluid of patients with endometriosis. , 1997, Human reproduction.

[5]  L. Carson,et al.  Prevention of postoperative adhesions by an antibody to vascular permeability factor/vascular endothelial growth factor in a murine model. , 1996, American journal of obstetrics and gynecology.

[6]  M. Frazier-Jessen,et al.  Estrogen suppression of connective tissue deposition in a murine model of peritoneal adhesion formation. , 1996, Journal of immunology.

[7]  M. Frazier-Jessen,et al.  Estrogen regulation of JE/MCP‐1 mRNA expression in fibroblasts , 1996, Journal of leukocyte biology.

[8]  E. Kovacs,et al.  Modulation of JE/MCP-1 expression in dermal wound repair. , 1995, The American journal of pathology.

[9]  E. Kovacs,et al.  Fibrogenic cytokines and connective tissue production , 1994, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[10]  R. Strieter,et al.  Production of monocyte chemoattractant protein-1 and macrophage inflammatory protein-1 alpha by inflammatory granuloma fibroblasts. , 1994, The American journal of pathology.

[11]  L. Gold,et al.  Localization of transforming growth factor beta isoforms TGF-beta 1, TGF-beta 2, and TGF-beta 3 in surgically induced pelvic adhesions in the rat. , 1994, Obstetrics and gynecology.

[12]  J. Brieland,et al.  Expression of monocyte chemoattractant protein-1 (MCP-1) by rat alveolar macrophages during chronic lung injury. , 1993, American Journal of Respiratory Cell and Molecular Biology.

[13]  Ray Nf,et al.  Economic impact of hospitalizations for lower abdominal adhesiolysis in the United States in 1988. , 1993 .

[14]  A. Fogelman,et al.  Monocytes may amplify their recruitment into inflammatory lesions by inducing monocyte chemotactic protein. , 1992, Arteriosclerosis and thrombosis : a journal of vascular biology.

[15]  S. Coughlin,et al.  Monocyte chemoattractant protein-1 in human atheromatous plaques. , 1991, The Journal of clinical investigation.

[16]  I. Otterness,et al.  The effect of interleukin-1 on adhesion formation in the rat. , 1991, American journal of obstetrics and gynecology.

[17]  B. Rollins,et al.  Recombinant human MCP-1/JE induces chemotaxis, calcium flux, and the respiratory burst in human monocytes. , 1991, Blood.

[18]  E. Kovacs Fibrogenic cytokines: the role of immune mediators in the development of scar tissue. , 1991, Immunology today.

[19]  Gary R. Grotendorst,et al.  Cloning and sequencing of a new gro transcript from activated human monocytes: expression in leukocytes and wound tissue , 1990, Molecular and cellular biology.

[20]  E. Leonard,et al.  Secretion by human fibroblasts of monocyte chemoattractant protein-1, the product of gene JE. , 1990, Journal of immunology.

[21]  G. diZerega The peritoneum and its response to surgical injury. , 1990, Progress in clinical and biological research.

[22]  R. Strieter,et al.  Monocyte chemotactic protein gene expression by cytokine-treated human fibroblasts and endothelial cells. , 1989, Biochemical and biophysical research communications.

[23]  K. Rodgers,et al.  The mitogenic activity of peritoneal tissue repair cells: control by growth factors. , 1989, The Journal of surgical research.

[24]  A. Decherney,et al.  The American Fertility Society classifications of adnexal adhesions, distal tubal occlusion, tubal occlusion secondary to tubal ligation, tubal pregnancies, müllerian anomalies and intrauterine adhesions. , 1988, Fertility and sterility.

[25]  M. Diamond,et al.  Pathogenesis of adhesion formation/reformation: Application to reproductive pelvic surgery , 1987, Microsurgery.

[26]  R. Nakamura,et al.  Modulation of fibroblast proliferation and transformation by activated macrophages during postoperative peritoneal reepithelialization. , 1986, American journal of obstetrics and gynecology.

[27]  R. Kistner,et al.  Revised American Fertility Society classification of endometriosis: 1985. , 1985, Fertility and sterility.

[28]  E. Wallach,et al.  Prevention and management of peritoneal adhesions. , 1984, Fertility and sterility.

[29]  Brent H. Cochran,et al.  Molecular cloning of gene sequences regulated by platelet-derived growth factor , 1983, Cell.

[30]  R. Buckman,et al.  A physiologic basis for the adhesion-free healing of deperitonealized surfaces. , 1976, The Journal of surgical research.

[31]  D. Milligan,et al.  Observations on the pathogenesis of peritoneal adhesions: a light and electron microscopical study , 1974, The British journal of surgery.

[32]  M. Weibel,et al.  Peritoneal adhesions and their relation to abdominal surgery. A postmortem study. , 1973, American journal of surgery.

[33]  G. Majno,et al.  Mesothelial injury and recovery. , 1973, The American journal of pathology.

[34]  E. Yonehiro,et al.  Intestinal Obstruction Caused by Adhesions: A Review of 388 Cases* , 1955, Annals of surgery.