Document Detail


Differential TNF production by monocyte subsets under physical stress: blunted mobilization of proinflammatory monocytes in prehypertensive individuals.
MedLine Citation:
PMID:  23046723     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Elevated blood pressure (BP) and infiltration of the vasculature by monocytes contribute to vascular pathology; but, monocyte migratory characteristics based on differing inflammatory potential under adrenergic activation remains unclear. We compared nonclassical (CD14(+)CD16(++); HLA-DR(+)), intermediate (CD14(++)CD16(+); HLA-DR(++)), and classical (CD14(++)CD16(-); HLA-DR(+/-)) monocyte trafficking and their LPS-stimulated TNF production in response to a physical stressor (20-min treadmill exercise at 65-70% VO(2peak)) in participants with high prehypertension (PHT), mild PHT or normal BP (NBP). To determine adrenergic receptor (AR) sensitivity, pre-exercise cells were also treated with isoproterenol (Iso). When cells were stimulated with LPS, the CD16 molecules were downregulated, and monocyte subsets were differentiated based on HLA-DR expression. Monocyte subpopulations (as % of total monocytes) and intracellular TNF production were evaluated by flow cytometry. TNF production in all subsets decreased post-exercise and with ex-vivo incubation with Iso, irrespective of BP (p<0.001), with nonclassical and intermediate monocytes being a major source of TNF production. Overall, % nonclassical monocytes increased, % intermediate did not change, whereas % classical decreased post-exercise (p<0.001). However, % increase in nonclassical monocytes under exercise-induced adrenergic activation was blunted in high PHT individuals (p<0.05), but not in individuals with mild PHT and NBP. These findings extend our previous reports by showing that the mobilization of proinflammatory monocytes under physical stress is attenuated with even mild BP elevation. This may be indicative of monocytic AR desensitization and/or greater adhesion of "proinflammatory" monocytes to the vascular endothelium in hypertension with potential clinical implications of vascular pathology.
Authors:
Stoyan Dimitrov; Farah Shaikh; Christopher Pruitt; Michael Green; Kathleen Wilson; Nuzhat Beg; Suzi Hong
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Publication Detail:
Type:  Journal Article; Research Support, American Recovery and Reinvestment Act; Research Support, N.I.H., Extramural     Date:  2012-10-06
Journal Detail:
Title:  Brain, behavior, and immunity     Volume:  27     ISSN:  1090-2139     ISO Abbreviation:  Brain Behav. Immun.     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2012-12-10     Completed Date:  2013-05-23     Revised Date:  2014-01-09    
Medline Journal Info:
Nlm Unique ID:  8800478     Medline TA:  Brain Behav Immun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  101-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Adult
Antigens, CD14 / immunology
Case-Control Studies
Cell Differentiation / drug effects,  immunology
Cell Movement / drug effects,  immunology
Down-Regulation
Exercise / physiology*
Exercise Test
Female
Flow Cytometry
GPI-Linked Proteins / drug effects,  immunology
HLA-DR Antigens / immunology
Humans
Isoproterenol / pharmacology
Lipopolysaccharides / immunology,  pharmacology*
Male
Monocytes* / cytology,  drug effects,  immunology
Prehypertension / immunology*
Receptors, Adrenergic / drug effects,  immunology
Receptors, IgG / drug effects,  immunology
Sympathomimetics / pharmacology
Tumor Necrosis Factor-alpha / drug effects,  immunology*
Grant Support
ID/Acronym/Agency:
HL090975S1/HL/NHLBI NIH HHS; R01 HL090975/HL/NHLBI NIH HHS; R01HL090975/HL/NHLBI NIH HHS; UL1 RR031980/RR/NCRR NIH HHS; UL1RR031980/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD14; 0/FCGR3B protein, human; 0/GPI-Linked Proteins; 0/HLA-DR Antigens; 0/Lipopolysaccharides; 0/Receptors, Adrenergic; 0/Receptors, IgG; 0/Sympathomimetics; 0/Tumor Necrosis Factor-alpha; L628TT009W/Isoproterenol
Comments/Corrections

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