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Updated: Jun 19, 2026
Bioengineering of Humanized Bone Marrow Microenvironments in Mouse and Their Visualization by Live Imaging
Published on: August 1, 2017
In vitro activation of human peripheral blood mononuclear cells induced by human biologic meshes
Sean Orenstein1, Yi Qiao, Manjot Kaur
1Connecticut Comprehensive Center for Hernia Repair, Department of Surgery, University of Connecticut Health Center, Farmington, Connecticut 06030, USA.
Background:
Inflammation and wound healing play critical roles in the integration of biologic meshes (BMs) at sites of hernia repair. Monocytes/macrophages (M/MQs) are key cells involved in mesh integration. Interleukin-1beta (IL-1beta) is one of the major M/MQ-derived cytokines, and its expression is a reflection of the degree of M/MQ activation. We hypothesized that BMs induce M/MQ activation in vitro and that IL-1beta expression by M/MQ varies among various BMs.
Materials And Methods:
Acellular human dermis-derived BM samples (AlloDerm, AlloMax, FlexHD) were placed in 48-well plates and cultured with peripheral blood mononuclear cells (PBMCs) from three healthy human subjects for 7 d. The resulting supernatants were assayed for IL-1beta levels by enzyme-linked immunosorbent assay (ELISA), and the BMs were evaluated histologically.
Results:
IL-1beta expression varied among donors as well as the BMs [AlloDerm (2.11-38.25pg/10(6) PBMCs); AlloMax (13.12-715.40pg/10(6) PBMCs); and FlexHD (116.69-665.40pg/10(6) PBMCs)]. Analysis of this data indicated that AlloMax and FlexHD induced significantly more M/MQ activation compared with AlloDerm (P<0.05). Histologic evaluation of the BMs indicated adherence of M/MQs on BM surface, however no degradation was detected.
Conclusion:
For the first time, we have demonstrated that M/MQs are activated to varying levels by human BMs in vitro. These differences may be related to BM processing technologies and/or the biologic variation between donors. Our results raise the possibility that these differences in M/MQ activation could result in varying intensity of inflammation and wound healing that control the integration of BMs at sites of hernia repair.
