Anzeige
Erschienen in:
01.03.2011 | Original Article
Chronological evaluation of inflammatory mediators during peritoneal adhesion formation using a rat model
Erschienen in: Langenbeck's Archives of Surgery | Ausgabe 3/2011
Einloggen, um Zugang zu erhaltenAbstract
Purpose
The inflammatory response to peritoneal injury is considered to be of particular importance in adhesion formation. The aim of this study was to investigate the dynamics of inflammatory mediators in peritoneal adhesions.
Methods
In 60 male rats, a peritoneal defect was performed using a standardized cecal abrasion model. On days 3, 5, 14, 30, 60, and 90, ten animals were sacrificed. The expression of five integral mediators for the cellular immune response (macrophages, T lymphocytes), inflammation (COX-2), cell differentiation, and proliferation (ß-catenin, c-myc) in visceral and parietal adhesions were analyzed.
Results
A distinct infiltration of macrophages was observed in all animals up to the 90th postoperative day with a peak on day 3 for visceral adhesions (26.3 ± 5.6%) and on day 14 for parietal adhesions (5.1 ± 1.1%). Compared to parietal adhesions, macrophage levels were significantly higher on day 3 (p = 0.001) and 5 (p = 0.002) but significantly lower on days 30, 60, and 90 in visceral adhesions (p = 0.041; p = 0.001; p = 0.017). T lymphocytes were detected over time with the highest levels on day 3 (visceral 4.0 ± 0.7%; parietal 6.7 ± 2.9%). High levels of COX-2 expression could be detected for the whole observation period. Positive expression of both ß-catenin and c-myc was detected in persistent adhesions; however, no expression of c-myc was observed in parietal adhesions.
Conclusions
The inflammatory reaction in adhesions is not limited to the early postoperative phase. Macrophages may be fundamental in triggering adhesions, and the presence of T cells indicates an additional role of the adoptive immune system. Identification of chemokines and chemokine receptors that trigger the cellular immune response might be a potential option to minimize adhesion formation.