Tumor necrosis factor α, protein gene product 9.5, matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 presence in congenital intra-abdominal adhesions in children under one year of age.

Abstract

IntroductionThe regulatory role of cytokines and extracellular matrix remodeling factors in congenital intra-abdominal adhesions has not yet been defined. The aim of this study was to assess the presence and relative distribution of tumor necrosis factor α (TNF-α), protein gene product 9.5 (PGP 9.5), matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) in adhesions.Material and methodsTNF-α, PGP 9.5, MMP-2 and TIMP-2 were detected using immunohistochemical methods and their relative distribution was evaluated by means of the semiquantitative counting method. The results were analyzed using non-parametric statistical methods.ResultsA moderate number of TNF-α positive macrophages and fibroblasts was found. A positive correlation was observed between the immunoreactive structures for TNF-α and PGP 9.5. A positive reaction for PGP 9.5 was observed in nerve fibers and shape modified fibroblasts. In control group tissues, positive structures were seen in significantly higher counts for PGP 9.5. Few to moderate numbers of MMP-2 positive macrophages, epithelioid cells, fibroblasts and endotheliocytes were detected. There was no significant difference between the groups. A positive reaction for TIMP-2 was seen in fibroblasts, macrophages and endotheliocytes. In control group tissues, positive structures were found in significantly higher counts for TIMP-2.ConclusionsThe positive correlation between the immunoreactive structures for TNF-α and PGP 9.5 suggests that nerve in-growth into intraabdominal adhesions might be induced by TNF-α and PGP 9.5 could have a role in maintaining inflammation. The down-regulation of PGP 9.5 suggests that pathogenesis of congenital intraabdominal adhesions may be related to hypoxia induced damage. The imbalance between MMP-2 and TIMP-2 may prove tissue fibrosis as a response to congenital peritoneal adhesions.