ADSC-conditioned media elicit an ex vivo anti-inflammatory macrophage response. (November 2018)

• Record Type: Journal Article
• Authors: Kruger, Maria Jacoba; Conradie, Maria Martha; Conradie, Magda; van de Vyver, Mari
• Is Part Of: Journal of molecular endocrinology. Volume 61:Number 4(2018)
• Page Start: 173
• Page End: 184
• Publication Date: 2018-11
• Subjects: macrophages -- Pentraxin3 -- obesity -- interleukin 10 -- metabolic syndrome; Molecular endocrinology -- Periodicals; Endocrinology -- Periodicals; 616.407
• DOI: 10.1530/JME-18-0078
• Languages: English
• ISSNs: 0952-5041

Abstract

Abstract : Obesity-associated inflammatory mechanisms play a key role in the pathogenesis of metabolic-related diseases. Failure of anti-inflammatory control mechanisms within adipose tissue and peripheral blood mononuclear cells (PBMCs) have been implicated in disease progression. This study investigated the efficacy of allogeneic adipose tissue-derived mesenchymal stem cells conditioned media (ADSC-CM) to counteract persistent inflammation by inducing an anti-inflammatory phenotype and cytokine response within PBMCs derived from patients with and without metabolic syndrome. Forty-six ( n = 46) mixed ancestry females (18–45 years) were subdivided into (a) healthy lean (HL) ( n = 10) (BMI <25 kg/m 2 ), (b) overweight/obese (OW/OB) (BMI ≥25 kg/m 2, <3 metabolic risk factors) ( n = 22) and (c) metabolic syndrome (MetS) (visceral adiposity, ≥3 metabolic risk factors) ( n = 14) groups. Body composition (DXA scan), metabolic (cholesterol, HDL, LDL, triglycerides, blood glucose) and inflammatory profiles (38-Plex cytokine panel) were determined. PBMCs were isolated from whole blood and treated ex vivo with either (i) autologous participant-derived serum, (ii) ADSCs-CM or (iii) a successive treatment regime. The activation status (CD11b+) and intracellular cytokine (IL6, IL10, TNFa) expression were determined in M1 (CD68+CD206−CD163−) and M2 (CD68+CD163+ CD206+) macrophage populations using flow cytometry. ADSC-CM treatment, promoted a M2 macrophage phenotype and induced IL10 expression, this was most pronounced in the OW/OB group. This response is likely mediated by multiple complementing factors within ADSC-CM, yet to be identified. This study is the first to demonstrate the therapeutic potential of ADSC-CM to restore the inflammatory balance in immune compromised obese individuals.