OBJECTIVE: Intraperitoneal adhesions are a significant cause of morbidity among women of reproductive age. Monocyte chemotactic protein 1 plays a role in the chemotaxis of mononuclear cells and fibroblasts into the peritoneal injury site. To evaluate its role in intraperitoneal adhesion formation, we used an established postsurgical adhesion model in mice. STUDY DESIGN: Surgical adhesions in mice were induced by scraping and crushing peritoneal sites. We analyzed the injury sites for the temporal expression of monocyte chemotactic protein 1 messenger ribonucleic acid and cellular infiltration at 12 to 24 hours across 10 days and evaluated the effects of monocyte chemotactic protein 1 and anti-monocyte chemotactic protein 1 neutralizing antibody on adhesion formation. On induction of adhesions animals were randomly assigned to 1 of 4 groups: (1) control, (2) nonspecific immunoglobulin G, (3) monocyte chemotactic protein 1, (4) anti-monocyte chemotactic protein 1 antibody. Animals received daily intraperitoneal injections for 6 days. Adhesions were scored on day 14 and immunostained for fibroblasts and macrophages. RESULTS: Adhesions developed consistently by the fifth postoperative day. We detected an increase in monocyte chemotactic protein 1 messenger ribonucleic acid expression at 48 hours; this remained until the fourth postoperative day. By the second day macrophages were present at the injury site. Animals treated with anti-monocyte chemotactic protein 1 antibody had significantly fewer adhesions develop than did the other three groups. CONCLUSION: This study demonstrates that monocyte chemotactic protein 1 may play a role in adhesion formation. Inhibiting the action of this chemokine may help to prevent adhesions.
OBJECTIVE: Intraperitoneal adhesions are a significant cause of morbidity among women of reproductive age. Monocyte chemotactic protein 1 plays a role in the chemotaxis of mononuclear cells and fibroblasts into the peritoneal injury site. To evaluate its role in intraperitoneal adhesion formation, we used an established postsurgical adhesion model in mice. STUDY DESIGN: Surgical adhesions in mice were induced by scraping and crushing peritoneal sites. We analyzed the injury sites for the temporal expression of monocyte chemotactic protein 1 messenger ribonucleic acid and cellular infiltration at 12 to 24 hours across 10 days and evaluated the effects of monocyte chemotactic protein 1 and anti-monocyte chemotactic protein 1 neutralizing antibody on adhesion formation. On induction of adhesions animals were randomly assigned to 1 of 4 groups: (1) control, (2) nonspecific immunoglobulin G, (3) monocyte chemotactic protein 1, (4) anti-monocyte chemotactic protein 1 antibody. Animals received daily intraperitoneal injections for 6 days. Adhesions were scored on day 14 and immunostained for fibroblasts and macrophages. RESULTS: Adhesions developed consistently by the fifth postoperative day. We detected an increase in monocyte chemotactic protein 1 messenger ribonucleic acid expression at 48 hours; this remained until the fourth postoperative day. By the second day macrophages were present at the injury site. Animals treated with anti-monocyte chemotactic protein 1 antibody had significantly fewer adhesions develop than did the other three groups. CONCLUSION: This study demonstrates that monocyte chemotactic protein 1 may play a role in adhesion formation. Inhibiting the action of this chemokine may help to prevent adhesions.
Authors: Jarosław Cwalinski; Ryszard Staniszewski; Ewa Baum; Tomasz Jasinski; Beata Mackowiak; Andrzej Bręborowicz Journal: Int J Clin Exp Med Date: 2015-06-15