The aim of the study was to investigate the immune-modulatory potential of commercially available PTFE and polyester vascular grafts with and without gelatine-coating. The biomaterial-cell-interaction was characterized by changes of established parameters such as PMN-related receptors/mediators, phagocytosis potential and capacity as well as the effect of an additional plasma-dependent modulation.
Material and methods. By means of a standardized experimental in vitro model, various vascular graft material (PTFE/polyester/uncoated/gelatine-coated) was used for incubation with or without plasma and co-culturing with human neutrophile granulocytes (PMN) followed by analysis of representative receptors and mediators (CD62L, CD11b, CXCR2, fMLP-R, IL-8, Elastase, LTB4). Oxidative burst assessed phagocytosis capacity.
Results. Comparing the vascular grafts, un-coated PTFE induced the lowest magnitude of cell stimulation whereas in case of gelatine-coating, cell response exceeded those of the other vascular grafts. This was also found comparing the polyester-based prosthetic material. Gelatine-coated polyester led to a more pronounced release of elastase than gelatine-coated PTFE and the uncoated materials. The results of oxidative burst indicated a reduced phagocytosis capacity in case of gelatine-coated polyester. Plasma incubation did also provide an impact on the cellular response. While in case of gelatine-coating, PMN-related receptor stimulation became lower, it increased by native polyester. The latter one did also induce more mediators such as IL-8 and LTB4 than gelatine-coated material.
Conclusions. There have been no extensive data on cell-cell interactions, cytokines and general histo-/hemocompatibility of human cells by the new generation of vascular grafts. It remains still open whether healing process and infectious resistance can be compromised by material-dependent over-stimulation or reduced phagocytosis potential of the immune cells of the primary unspecific immune response induced by gelatine-coated materials.