This is the Scientific Surgery Archive, which contains all randomized clinical trials in surgery that have been identified by searching the top 50 English language medical journal issues since January 1998. Compiled by Jonothan J. Earnshaw, former Editor-in-Chief, BJS

Interferon γ and plasminogen activator inhibitor 1 regulate adhesion formation after partial hepatectomy. BJS 2014; 101: 398-407.

Published: 17th February 2014

Authors: K. Ohashi, T. Yoshimoto, H. Kosaka, T. Hirano, Y. Iimuro, K. Nakanishi et al.

Background

The pathophysiology of intra‐abdominal adhesions has not been studied extensively. The aim of this study was to elucidate the molecular mechanisms underlying adhesion formation in a murine model and in patients undergoing hepatectomy.

Method

Partial hepatectomy was performed using bipolar forceps in mice. Wild‐type mice, antibodies to CD4 and interferon (IFN) γ, IFN‐γ, natural killer T (NKT) cells and plasminogen activator inhibitor (PAI) 1 knockout (KO) mice were used. Recombinant hepatocyte growth factor (HGF) was tested for its ability to prevent adhesions. Liver specimens were obtained during surgery from patients undergoing hepatectomy. Adhesion formation was evaluated using a scoring system that ranged from 0 (no adhesions) to 5 (severe adhesions). Levels of IFN‐γ and PAI‐1 mRNA, and protein concentration of PAI‐I were measured, and fluorescence immunostaining was performed.

Results

Adhesion formation depended on IFN‐γ produced by NKT cells, and NKT KO mice developed few adhesions (mean(s.d.) 1·7(0·3) versus 4·6(0·4) in wild‐type mice; P = 0·037). In wild‐type mice, the level of PAI‐1 mRNA increased after hepatectomy, followed by a decrease in the tissue plasminogen activator (tPA) mRNA level. Adhesion formation was inhibited completely in PAI‐1 KO mice (0(0) versus 4·1(0·8) in wild‐type mice; P = 0·002). HGF inhibited formation of abdominal adhesions after hepatectomy by reducing IFN‐γ and PAI‐1 levels, and increasing tPA levels compared with those in mice treated with phosphate‐buffered saline (P < 0·001, P = 0·002 and P = 0·035 respectively). In human liver specimens, NKT cells accumulated in the liver after hepatectomy, and PAI‐1 expression was increased 5·25‐fold (P = 0·030).

Conclusion

IFN‐γ is a key molecule for abdominal adhesion formation after hepatectomy, acting via the reciprocal balance of PAI‐1 and tPA. This molecular mechanism may also regulate adhesion formation in patients following hepatectomy. HGF inhibited formation of adhesions by regulating IFN‐γ and PAI‐1, suggesting that it may be an important target for prevention of adhesions after hepatectomy.

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