The role of neutrophils in peritoneal adhesion formation

Aamer Ar'rajab, William Mileski, James T. Sentementes, Patricia Sikes, Richard B. Harris, Ingemar J A Dawidson

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

The most common cause of intraperitoneal adhesions is previous abdominal surgery. Postoperative adhesion formation results from a fibroproliferative inflammatory reaction that begins with an influx of polymorphonuclear leukocytes (PMNs) into the peritoneal cavity. Adherence of the PMNs to the endothelial cells (EC) is necessary for PMN migration into the tissue in response to a stimulus. Several receptor-counterreceptor pairs of ligands such as CD11/CD18 on the PMN and ICAM-1 (CD54) on EC have been identified. Monoclonal antibody against CD11/CD18 (R15.7) inhibits PMN adherence and migration and consequently protects against PMN-induced tissue injuries. We therefore studied the effect of preventing PMN-EC adherence, using anti-CD18 monoclonal antibody, on postoperative adhesion formation in rabbits. Group 1 was a control receiving physiologic saline, and group 2 received anti-CD18 antibody (R15.7, 2 mg/kg). The treatment was administered iv at the end of surgery and repeated on the first and second postoperative days. Peritoneal adhesions were induced at laparotomy by repairing two peritoneal defects, by oversewing the defect (model 1), and by resuturing the removed parietal peritoneum in its place as an ischemic graft (model 2). Adhesions were evaluated blindly at 10 days after operation by measuring the percentage of the suture line covered with adhesions (model 1) or by a scoring system (model 2). All control animals developed intraperitoneal adhesions and the percentage of the suture line covered with adhesions was 25 ± 5.9% (mean ± SEM) and the mean score in model 2 was 0.9 ± 0.2. Anti-CD18 antibody, R15.7, increased the degree of postoperative adhesion formation in both models, but the results were significant only in model 2. Also, anti-CD18 antibody significantly decreased peritoneal neutrophils from 11.1 x 107 ± 1.8 x 107 to 2.2 x 107 ± 0.4 x 107 (P < 0.001) on the first postoperative day. It is concluded that inhibition of PMN-EC adherence does influence the postoperative adhesion formation. These results might suggest that PMNs have a role in modulating postoperative adhesion formation.

Original languageEnglish (US)
Pages (from-to)143-146
Number of pages4
JournalJournal of Surgical Research
Volume61
Issue number1
DOIs
StatePublished - Feb 15 1996
Externally publishedYes

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Neutrophils
Endothelial Cells
Anti-Idiotypic Antibodies
Sutures
Monoclonal Antibodies
Peritoneum
Peritoneal Cavity
Intercellular Adhesion Molecule-1
Laparotomy
Rabbits
Ligands
Transplants
Wounds and Injuries

ASJC Scopus subject areas

  • Surgery

Cite this

Ar'rajab, A., Mileski, W., Sentementes, J. T., Sikes, P., Harris, R. B., & Dawidson, I. J. A. (1996). The role of neutrophils in peritoneal adhesion formation. Journal of Surgical Research, 61(1), 143-146. https://doi.org/10.1006/jsre.1996.0095

The role of neutrophils in peritoneal adhesion formation. / Ar'rajab, Aamer; Mileski, William; Sentementes, James T.; Sikes, Patricia; Harris, Richard B.; Dawidson, Ingemar J A.

In: Journal of Surgical Research, Vol. 61, No. 1, 15.02.1996, p. 143-146.

Research output: Contribution to journalArticle

Ar'rajab, A, Mileski, W, Sentementes, JT, Sikes, P, Harris, RB & Dawidson, IJA 1996, 'The role of neutrophils in peritoneal adhesion formation', Journal of Surgical Research, vol. 61, no. 1, pp. 143-146. https://doi.org/10.1006/jsre.1996.0095
Ar'rajab A, Mileski W, Sentementes JT, Sikes P, Harris RB, Dawidson IJA. The role of neutrophils in peritoneal adhesion formation. Journal of Surgical Research. 1996 Feb 15;61(1):143-146. https://doi.org/10.1006/jsre.1996.0095
Ar'rajab, Aamer ; Mileski, William ; Sentementes, James T. ; Sikes, Patricia ; Harris, Richard B. ; Dawidson, Ingemar J A. / The role of neutrophils in peritoneal adhesion formation. In: Journal of Surgical Research. 1996 ; Vol. 61, No. 1. pp. 143-146.
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abstract = "The most common cause of intraperitoneal adhesions is previous abdominal surgery. Postoperative adhesion formation results from a fibroproliferative inflammatory reaction that begins with an influx of polymorphonuclear leukocytes (PMNs) into the peritoneal cavity. Adherence of the PMNs to the endothelial cells (EC) is necessary for PMN migration into the tissue in response to a stimulus. Several receptor-counterreceptor pairs of ligands such as CD11/CD18 on the PMN and ICAM-1 (CD54) on EC have been identified. Monoclonal antibody against CD11/CD18 (R15.7) inhibits PMN adherence and migration and consequently protects against PMN-induced tissue injuries. We therefore studied the effect of preventing PMN-EC adherence, using anti-CD18 monoclonal antibody, on postoperative adhesion formation in rabbits. Group 1 was a control receiving physiologic saline, and group 2 received anti-CD18 antibody (R15.7, 2 mg/kg). The treatment was administered iv at the end of surgery and repeated on the first and second postoperative days. Peritoneal adhesions were induced at laparotomy by repairing two peritoneal defects, by oversewing the defect (model 1), and by resuturing the removed parietal peritoneum in its place as an ischemic graft (model 2). Adhesions were evaluated blindly at 10 days after operation by measuring the percentage of the suture line covered with adhesions (model 1) or by a scoring system (model 2). All control animals developed intraperitoneal adhesions and the percentage of the suture line covered with adhesions was 25 ± 5.9{\%} (mean ± SEM) and the mean score in model 2 was 0.9 ± 0.2. Anti-CD18 antibody, R15.7, increased the degree of postoperative adhesion formation in both models, but the results were significant only in model 2. Also, anti-CD18 antibody significantly decreased peritoneal neutrophils from 11.1 x 107 ± 1.8 x 107 to 2.2 x 107 ± 0.4 x 107 (P < 0.001) on the first postoperative day. It is concluded that inhibition of PMN-EC adherence does influence the postoperative adhesion formation. These results might suggest that PMNs have a role in modulating postoperative adhesion formation.",
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