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Inflammatory Circulating Mononuclear Cell Phenotype in Healthy Older Adults with Low‐Grade Systemic Inflammation and Endothelial Dysfunction
Author(s) -
Gano Lindsey B,
Magerko Katie A.,
Roeca Cassandra,
Lawson Brooke R.,
Jablonski Kristen L.,
Seals Douglas R.,
Donato Anthony J.
Publication year - 2008
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.22.1_supplement.1155.4
Subject(s) - inflammation , medicine , endocrinology , peripheral blood mononuclear cell , tumor necrosis factor alpha , monocyte , systemic inflammation , endothelial dysfunction , receptor , western blot , pathophysiology , immunology , chemistry , biochemistry , in vitro , gene
Chronic low‐grade inflammation may contribute to vascular endothelial dysfunction with aging. Changes in the inflammatory properties of circulating mononuclear cells (MC) may be involved, but data are limited. Compared with young controls (Y, 25±2 yr, n=9), healthy older adults (O, 65±2 yr, n=12) had elevated plasma concentrations of C‐reactive protein (0.85±0.15 vs. 0.42±0.10 mg/L, P<0.05) and interleukin‐6 (IL‐6, 1.32±0.22 vs. 0.64 ±0.05 pg/ml, P<0.05), and reduced maximal forearm blood flow responses to acetylcholine (12.8±1.3 vs. 17.9±2.2 mL tissue −1 min −1 , P<0.05). MC mRNA expression (real‐time RT PCR) of inflammatory cytokines monocyte chemoattractant protein‐1 (MCP‐1, 1.52±0.34 vs. 0.00±0.42 Fold change from Y[FC], P<0.05), tumor necrosis factor α (TNF‐α, 2.68±0.50 vs. 0.00±0.34 FC, P<0.05) and IL‐6 (1.98±0.91 vs. 0.00±0.83 FC, P=0.07) were greater, whereas the anti‐inflammatory nuclear transcription factor peroxisome proliferator activated receptor α (PPAR‐α, −1.28±0.50 vs. 0.00±0.51 FC, P<0.05) was lower in O. MC protein expression (Western blot analysis) of inflammatory molecules MCP‐1, TNF‐α and IL‐6 also was greater in a subgroup of O vs. Y. These preliminary results provide evidence that MC of healthy older adults exhibit a pro‐inflammatory phenotype that may contribute to chronic low‐grade systemic inflammation and vascular endothelial dysfunction with aging. NIH AG006537 , AG013038 , AG022241