Polypropylene meshes that are commonly used for
inguinal hernia repair may trigger granulomatous
foreign body reactions. Here, we show that asymptomatic patients display mesh-associated inflammatory
granulomas long after surgery, which are dominated by monocyte-derived macrophages expressing high levels of inflammatory activation markers. In mice, mesh implantation by the onlay technique induced rapid and strong myeloid cell accumulation, without substantial attenuation for up to 90 days. Myeloid cells segregated into distinct macrophage subsets with separate spatial distribution, activation profiles, and functional properties, showing a stable inflammatory phenotype in the tissue surrounding the
biomaterial and a mixed, wound-healing phenotype in the surrounding stromal tissue.
Protein mass spectrometry confirmed the inflammatory nature of the
foreign body reaction, as characterized by
cytokines, complement activation, and matrix-modulating factors. Moreover,
immunoglobulin deposition increased over time around the implant, arguing for humoral immune responses in association with the cell-driven
inflammation. Intravital multiphoton microscopy revealed a high motility and continuous recruitment of myeloid cells, which is partly dependent on the
chemokine receptor CCR2. CCR2-dependent macrophages are particular drivers of fibroblast proliferation. Thus, our work functionally characterizes myeloid cell-dependent
inflammation following mesh implantation, thereby providing insights into the dynamics and mechanisms of
foreign body reactions to implanted
biomaterials.