Possible Role of Natural Immune Response against Altered Fibroblasts in the Development of Post-Operative Adhesions
Article first published online: 3 MAY 2006
American Journal of Reproductive Immunology
Volume 55, Issue 6, pages 420–427, June 2006
How to Cite
Alpay, Z., Özgönenel, M. S., Savaşan, S., Buck, S., Saed, G. M. and Diamond, M. P. (2006), Possible Role of Natural Immune Response against Altered Fibroblasts in the Development of Post-Operative Adhesions. American Journal of Reproductive Immunology, 55: 420–427. doi: 10.1111/j.1600-0897.2006.00378.x
- Issue published online: 3 MAY 2006
- Article first published online: 3 MAY 2006
- Submitted November 28, 2005; accepted February 7, 2006.
- Intercellular adhesion molecule-1;
- natural immune response;
- post-operative adhesions;
- TNF-alpha receptor
Post-operative adhesion tissue fibroblasts (ATF) differ from normal peritoneal fibroblasts (NPF). Natural immune response participates in the elimination of altered cells. In this study, we investigated NPF and ATF expression patterns of immune response-related markers, and lymphokine-activated killer (LAK) cell-mediated fibroblast elimination in vitro.
Method of study
Primary cell cultures of both NPF and ATF obtained from the same four patients were used in the experiments. The expression of CD54, CD40 and CD120b, and allogeneic LAK cell-mediated ATF and NPF elimination were studied by flow cytometry.
Average expression of CD54 in ATF was greater by 12.3-fold compared with NPF (P = 0.021), with ratios of 2.4 and 1.9-fold for CD40 (P < 0.001) and CD120b (P = 0.013), respectively. Average LAK cell-mediated fibroblast killing was 1.8 ± 0.8-fold greater in ATF over NPF (P = 0.008). Furthermore, LAK cell-mediated fibroblast elimination correlated significantly with the increased CD40, CD54 and CD120b expression (R > 0.956; P < 0.05 for each).
These results demonstrate that ATF are more susceptible to lymphocyte-mediated elimination than NPF and the development of adhesions despite this could be explained by either impaired or overwhelmed autologous natural immune response against reactive fibroblasts.