M A Valtierra-Alvarado1, J E Castañeda Delgado2, S I Ramírez-Talavera1, G Lugo-Villarino3, F Dueñas-Arteaga4, A Lugo-Sánchez5, M S Adame-Villalpando5, B Rivas-Santiago6, J Enciso-Moreno6, C J Serrano7. 1. Unidad de Investigación Biomédica Zacatecas, Instituto Mexicano del Seguro Social, Mexico; Departamento de Inmunología, Centro de Investigación en Ciencias de la Salud y Biomedicina, Universidad Autónoma de San Luis Potosí (UASLP), Mexico. 2. Cátedras CONACyT, Consejo Nacional de Ciencia y Tecnología (CONACyT-México), Unidad de Investigación Biomédica Zacatecas, Instituto Mexicano del Seguro Social, Zacatecas, Mexico. 3. Institut de Pharmacologie et de Biologie Structurale, Université de Toulouse, CNRS, UPS, Toulouse, France. 4. Universidad Autónoma de Zacatecas, Unidad Académica de Medicina Humana y Ciencias de la Salud, Zacatecas, Mexico. 5. Unidad de Investigación Biomédica Zacatecas, Instituto Mexicano del Seguro Social, Mexico; Universidad Autónoma de Zacatecas, Unidad Académica de Ciencias Químicas, Zacatecas, Mexico. 6. Unidad de Investigación Biomédica Zacatecas, Instituto Mexicano del Seguro Social, Mexico. 7. Unidad de Investigación Biomédica Zacatecas, Instituto Mexicano del Seguro Social, Mexico. Electronic address: serranocj@imss.gob.mx.
Abstract
AIMS: Monocytes and macrophages express cell-surface markers indicative of their inflammatory and activation status. In this study, we investigated whether these markers are affected or correlated in non-obese T2D subjects, or glycemic/metabolic control variables. METHODS: Clinical data was recorded, and peripheral blood drawn from T2D patients (n = 28) and control subjects (n = 27). Isolated monocytes were evaluated by flow cytometry for the expression of CD14, CD16, and the phenotypic markers for the different states of activation spectrum, such as pro-inflammatory (M1) (HLA-DR, CD86), anti-inflammatory/pro-resolving (M2) (CD163, CD206, MERTK, PD-L1) and metabolically-activated (MMe) (CD36, ABCA-1). From a subset of individuals, monocytes-derived macrophages (MDM) were obtained and evaluated for phenotypic markers. A correlation analysis was performed between the clinical variables and the marker expression. RESULTS: The frequency of CD14++CD16- monocytes was lower in T2D patients and it correlates negatively with poor control in glycemic and metabolic variables. T2D monocytes expressed lower levels of HLA-DR, CD86, PD-L1, and CD163, which correlated negatively with poor metabolic control. In MDM from T2D patients, HLA-DR, CD86 and CD163 expression was lower and it inversely correlated with deficient glycemic or metabolic control parameters. CONCLUSION: The glycemic/metabolic control associated with T2D influences monocyte and MDM phenotypes toward an immune-suppressive phenotype.
AIMS: Monocytes and macrophages express cell-surface markers indicative of their inflammatory and activation status. In this study, we investigated whether these markers are affected or correlated in non-obese T2D subjects, or glycemic/metabolic control variables. METHODS: Clinical data was recorded, and peripheral blood drawn from T2D patients (n = 28) and control subjects (n = 27). Isolated monocytes were evaluated by flow cytometry for the expression of CD14, CD16, and the phenotypic markers for the different states of activation spectrum, such as pro-inflammatory (M1) (HLA-DR, CD86), anti-inflammatory/pro-resolving (M2) (CD163, CD206, MERTK, PD-L1) and metabolically-activated (MMe) (CD36, ABCA-1). From a subset of individuals, monocytes-derived macrophages (MDM) were obtained and evaluated for phenotypic markers. A correlation analysis was performed between the clinical variables and the marker expression. RESULTS: The frequency of CD14++CD16- monocytes was lower in T2D patients and it correlates negatively with poor control in glycemic and metabolic variables. T2D monocytes expressed lower levels of HLA-DR, CD86, PD-L1, and CD163, which correlated negatively with poor metabolic control. In MDM from T2D patients, HLA-DR, CD86 and CD163 expression was lower and it inversely correlated with deficient glycemic or metabolic control parameters. CONCLUSION: The glycemic/metabolic control associated with T2D influences monocyte and MDM phenotypes toward an immune-suppressive phenotype.