Objective: Diabetic women who receive polypropylene meshes in the surgical repair of stress urinary incontinence and/or pelvic organ prolapse have a ~5-fold increased risk in developing mesh complications, mainly mesh exposure and pain. Macrophage plays important roles in inflammation and mesh-tissue integration. This study aims to establish an association between diabetes and macrophage dysfunction at the mesh implantation site.
Methods: Diabetic (n=20) vs. nondiabetic (n=28) mesh-tissue complexes excised from women with mesh complications were assessed for macrophage phenotype transition, efferocytosis and immune mediator production with TUNEL apoptotic cell labeling, immunofluorescence, NanoString and Luminex multiplex assays. Significance of all statistical tests was set at 0.05 level.
Results: Demographic parameters were not different except that BMI was higher in diabetic women (p=0.04). In diabetic vs. nondiabetic specimens, the ratio of pro-healing M2 to pro-inflammatory M1 was 50% lower; the ratio of apoptotic cells/CD68+ macrophages was 50% higher; normal correlations of molecules involved in cell apoptosis (BCL10 and TRAF3) and CD68 were disrupted (Figure); and levels of chemokines CCL11, CCL13, CXCL10 were significantly increased (all p<0.05).
Conclusion: Diabetes was associated with macrophage dysfunction at the mesh implantation site, which may contribute to short-term and long-term mesh complications.
R. Liang: None. S. Lopa: None.
Pennsylvania Department of Health
