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NFKB and CCR2 gene expression reflect long‐term but not acute inflammatory activation of peripheral blood mononuclear cells in patients with type 2 diabetes (669.3)
Author(s) -
Horvath Peter,
RadomAizik Shlomit,
Oliver Stacy,
Zaldivar Frank,
Galassetti Pietro
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.669.3
Subject(s) - peripheral blood mononuclear cell , inflammation , medicine , type 2 diabetes , ccr2 , gene expression , endocrinology , immunology , diabetes mellitus , chemokine , gene , biology , biochemistry , chemokine receptor , in vitro
In type 2 diabetes (T2D) cardiovascular complications are linked to chronic inflammation, including activated granulocytes, Gc, and monocytes, Mc, present in atherosclerotic lesions. In T2D, hyperglycemia and hyperlipidemia are common, and can acutely activate Gc/Mc surface markers in healthy, obese, and T2D subjects. T2D also displays marked variability of inflammatory status, possibly reflecting long‐term modulation (often involving gene expression). We therefore compared, during 4‐h i.v. infusions of glucose, lipids, or glucose +lipids, acute leukocyte surface marker activation and peripheral blood mononuclear cell (PBMC’s) expression of the key inflammatory genes NFKB and CCR2 (by RT‐PCR) in 5 healthy, 5 obese, and 5 T2D subjects. Unlike cell surface markers, NFKB and CCR2 expression was not affected by acute plasma metabolite changes in any group, but levels of gene expression paralleled overall systemic inflammatory activation, which in T2D varied considerably within subjects across study visits, likely reflecting long‐term inflammatory modulation. Our data suggests a two‐tiered inflammatory mechanisms in T2D, with acute metabolic changes immediately reflected on surface marker expression, and more prolonged stimuli affecting levels of leukocyte inflammatory gene expression. Grant Funding Source : Supported by NIH Grants P01HD048721 and UL1RR031985