PMID- 24847781 OWN - NLM STAT- MEDLINE DCOM- 20150515 LR - 20171116 IS - 1557-8518 (Electronic) IS - 1540-4196 (Linking) VI - 12 IP - 7 DP - 2014 Sep TI - Monocytes from metabolic syndrome subjects exhibit a proinflammatory M1 phenotype. PG - 362-6 LID - 10.1089/met.2014.0017 [doi] AB - BACKGROUND: The metabolic syndrome is a highly prevalent state affecting one in three US adults and comprises a cluster of cardiometabolic risk factors. While metabolic syndrome is a proinflammatory state, there is a paucity of studies examining monocyte/macrophage phenotype in metabolic syndrome subjects. This was the aim of this study. METHODS: Following informed consent, metabolic syndrome and age- and gender-matched healthy subjects (n=15/group) were recruited, and monocytes were obtained for phenotypic characterization of the classical M1 phenotype and alternative M2 phenotype. Biomarkers of inflammation, C-reactive protein (CRP), and proinflammatory cytokines were examined. RESULTS: Metabolic syndrome subjects had significantly higher waist circumference (WC), significantly increased systolic blood pressure, higher fasting glucose, triglycerides, and free fatty acids levels, and lower high-density lipoprotein cholesterol (HDL-C) levels compared to matched controls. Also, CRP and endotoxin levels were significantly elevated in metabolic syndrome compared to controls. Metabolic syndrome subjects had significantly higher levels of the M1 phenotype and significantly decreased levels of the M2 phenotype compared to controls, even after adjusting for WC. Among the other biomarkers of inflammation, there were significant increases in the proinflammatory cytokines and chemokines interleukin-1beta (IL-1beta), IL-6, and monocyte chemoattractant protein-1 (MCP-1) and decreased IL-10 in metabolic syndrome compared to controls. The M1 phenotype was significantly correlated to levels of CRP, endotoxin, MCP-1, and WC and negatively with HDL-C. CONCLUSIONS: Monocytes from metabolic syndrome subjects display a proinflammatory M1 phenotype that could promote the increased cardiometabolic burden in these subjects. FAU - Chen, Xinpu AU - Chen X AD - Department of Pathology & Immunology, Baylor College of Medicine , and Texas Children's Hospital, Houston, Texas. FAU - Devaraj, Sridevi AU - Devaraj S LA - eng PT - Journal Article DEP - 20140521 PL - United States TA - Metab Syndr Relat Disord JT - Metabolic syndrome and related disorders JID - 101150318 RN - 0 (Biomarkers) RN - 0 (Cytokines) RN - 9007-41-4 (C-Reactive Protein) SB - IM MH - Adult MH - Biomarkers/metabolism MH - C-Reactive Protein/metabolism MH - Case-Control Studies MH - Cytokines/metabolism MH - Female MH - Humans MH - Inflammation/*blood/immunology MH - Male MH - Metabolic Syndrome/*blood/immunology MH - Middle Aged MH - Monocytes/classification/*immunology MH - Phenotype EDAT- 2014/05/23 06:00 MHDA- 2015/05/16 06:00 CRDT- 2014/05/23 06:00 PHST- 2014/05/23 06:00 [entrez] PHST- 2014/05/23 06:00 [pubmed] PHST- 2015/05/16 06:00 [medline] AID - 10.1089/met.2014.0017 [doi] PST - ppublish SO - Metab Syndr Relat Disord. 2014 Sep;12(7):362-6. doi: 10.1089/met.2014.0017. Epub 2014 May 21.