Andrea F Wise1, Timothy M Williams1, Stephen Rudd2, Christine A Wells3,4, Peter G Kerr5, Sharon D Ricardo1. 1. Department of Anatomy & Developmental Biology, Monash University, Clayton, Victoria, 3800, Australia. 2. Queensland Facility for Advanced Bioinformatics (QFAB), University of Queensland, St Lucia, Queensland, 4072, Australia. 3. The Australian Institute for Bioengineering & Nanotechnology, University of Queensland, St Lucia, Queensland, 4072, Australia. 4. Institute of Infection, Immunity & Inflammation, College of Medical, Veterinary & Life Sciences, University of Glasgow, Scotland, G12 8TA, UK. 5. Department of Medicine, Monash Medical Centre, Clayton, Victoria, 3168, Australia.
Abstract
AIM: Macrophage infiltration contributes to the pathogenesis of Type 2 diabetes. Mesenchymal stem cells (MSCs) possess immunomodulatory properties, making them an ideal candidate for therapeutic intervention. This study investigated whether MSCs can modulate the phenotype of monocytes isolated from Type 2 diabetic patients with end-stage renal disease. MATERIALS & METHODS: Monocytes from control (n = 4) and Type 2 diabetic patients with end-stage renal disease (n = 5) were assessed using flow cytometry and microarray profiling, following 48 h of co-culture with MSCs. RESULTS: Control subjects had a greater proportion of CD14(++)CD16(-) monocytes while diabetic patients had a higher proportion of CD14(++)CD16(+) and CD14(+)CD16(++) monocytes. MSCs promoted the proliferation of monocytes isolated from diabetic patients, reduced HLA-DR expression in both groups and promoted the expression of anti-inflammatory genes. CONCLUSION: MSC-derived factors alter the polarization of monocytes isolated from healthy and diabetic subjects toward an M2 phenotype.
AIM: Macrophage infiltration contributes to the pathogenesis of Type 2 diabetes. Mesenchymal stem cells (MSCs) possess immunomodulatory properties, making them an ideal candidate for therapeutic intervention. This study investigated whether MSCs can modulate the phenotype of monocytes isolated from Type 2 diabeticpatients with end-stage renal disease. MATERIALS & METHODS: Monocytes from control (n = 4) and Type 2 diabeticpatients with end-stage renal disease (n = 5) were assessed using flow cytometry and microarray profiling, following 48 h of co-culture with MSCs. RESULTS: Control subjects had a greater proportion of CD14(++)CD16(-) monocytes while diabeticpatients had a higher proportion of CD14(++)CD16(+) and CD14(+)CD16(++) monocytes. MSCs promoted the proliferation of monocytes isolated from diabeticpatients, reduced HLA-DR expression in both groups and promoted the expression of anti-inflammatory genes. CONCLUSION: MSC-derived factors alter the polarization of monocytes isolated from healthy and diabetic subjects toward an M2 phenotype.