Anti-interleukin-10: Effect on Postoperative Intraperitoneal Adhesion Formation in a Murine Model

Abstract

Despite the expenditure of millions of dollars in the development of agents intended to limit their occurrence, intraperitoneal adhesions remain a major source of surgery-related morbidity and mortality as well as a financial burden on Western health care systems [1, 2]. The inadequacies of presently available antiadhesion modalities probably arise from the inability or failure to employ evidence based on rational drug and device development, as much of what occurs at a molecular biologic level following the occurrence of a peritoneal injury is unknown. Drugs and devices such as barriers have often been selected based on their theoretical potential for success, and not on a thorough understanding of the cellular or molecular changes that lead to adhesion formation and what happens when these predictable changes are modified. Though the serial cellular events that transpire following a peritoneal injury have been defined [3], the exact role of cytokines in peritoneal repair and adhesion formation has only been partially elucidated. Preliminary data exist demonstrating that numerous cytokines such as interleukin (IL)-1 [4, 5], IL-2, transforming growth factor (TGF)-β, and platelet-derived growth factor (PDGF)-β [6] are potentiators of postoperative adhesion formation, while IL-10 (cytokine synthesis-inhibiting factor, CSIF) significantly inhibits such adhesion formation [7]. We proposed to confirm our prior findings regarding the adhesion prevention properties of IL-10.