Human monocyte activation by biologic and biodegradable meshes in vitro

Inflammation and wound healing play critical roles in the integration of biologic and biodegradable meshes (BMs) at hernia repair sites. Monocytes/macrophages (M/Ms) are key cells controlling inflammation and wound healing. These cells release inflammatory cytokines and growth factors such as interleukin (IL)-1 beta, IL-6, IL-8, and vascular endothelial growth factor (VEGF) upon activation. Although BMs have been increasingly used in hernia repairs worldwide, to date, investigations of inflammatory responses to various BMs have been limited. Mesh samples of three acellular human dermis-derived biologic meshes (AlloDerm, AlloMax, FlexHD) and one biodegradable synthetic mesh (Bio-A) were placed in 96-well plates. Human peripheral blood mononuclear cells (PBMCs) were isolated from six healthy subjects, added to each well, and incubated for 7 days. Culture supernatants were assayed for IL-1 beta, IL-6, IL-8, and VEGF levels using a multiplex bead-base immunoassay system (Bio-Plex). All four meshes induced cytokine expression from activated M/Ms to varying degrees in vitro. FlexHD induced significantly more IL-1 beta (2,591 pg/ml) than AlloMax (517 pg/ml), AlloDerm (48 pg/ml), or Bio-A (28 pg/ml) (p < 0.001). AlloMax stimulated a significantly greater quantity of IL-6 (38,343 pg/ml) than FlexHD (19,317 pg/ml), Bio-A (191 pg/ml), or AlloDerm (103 pg/ml) (p < 0.05). Interleukin-8 and VEGF displayed trends similar to that of IL-6. There were no significant differences in cytokine production between AlloDerm and Bio-A. This study demonstrated that human macrophages are activated by human dermis-derived biologic and biodegradable meshes in vitro. A wide range of cytokine and growth factor induction was seen among the different mesh products. These differences in M/M activation may be related to the proprietary processing technologies of the studied meshes. The study results raise the possibility that these differences in M/M activation could indicate varying intensities of inflammation that control integration of different biologic meshes at the sites of hernia repair.