Prolene-Monocryl-composite meshes do not increase microvascular Staphylococcus aureus adherence and do not sensitize...

Mesh implantation for hernia repair bears the risk of bacterial mesh infection. In this study, we analyzed whether this complication is supported by an increased interaction of bacteria and leukocytes with the microvascular endothelium at the implantation site.

Ultrapro meshes were implanted into the dorsal skinfold chamber of Syrian golden hamsters. After 12 days, fluorescein isothiocyanate (FITC)-labeled staphylococci were injected in the animals. Subsequently, we analyzed bacterial adherence, leukocyte-endothelial cell interaction, and microhemodynamics in venules of the mesh border zone and of distant control tissue under baseline conditions and during TNF-alpha-induced inflammation using intravital fluorescence microscopy. The results were compared to animals which did not receive any bacteria.

Under baseline conditions, leukocyte-endothelial cell interaction and bacterial adherence were not affected by the implanted biomaterial. TNF-alpha-induced inflammation significantly increased numbers of adherent leukocytes and bacteria in venules located in direct vicinity to the mesh however without any differences to control tissue. Comparable results were found for the leukocyte-endothelial cell interaction when animals were not exposed to bacteria.

Implanted Ultrapro meshes do neither increase microvascular Staphylococcus aureus adherence nor sensitize for leukocytic inflammation. Thus, we suggest that a mesh-induced increase of bacterial adherence in vessels of the implantation site cannot be considered as a primary cause for the development of mesh infection.