Document Detail


Pregravid obesity associates with increased maternal endotoxemia and metabolic inflammation.
MedLine Citation:
PMID:  20930711     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Obese pregnant women develop severe insulin resistance and enhanced systemic and placental inflammation, suggesting associated modifications of endocrine and immune functions. Activation of innate immunity by endotoxins/lipopolysaccharides (LPS) has been proposed as a mechanism for enhancing metabolic alterations in disorders with insulin resistance. The aim of this study was to characterize the immune responses developed by the adipose tissue (AT) and their potential links to maternal endotoxemia in pregnancy with obesity. Blood and subcutaneous abdominal AT were obtained from 120 lean and obese women (term pregnancy) recruited at delivery. Gene expression was assessed in AT and stromal vascular cells isolated from a subset of 24 subjects from the same cohort. Doubling of plasma endotoxin concentrations indicated subclinical endotoxemia in obese compared with lean women. This was associated with significant increase in systemic C-reactive protein and interleukin-6 (IL-6) but not tumor necrosis factor-α (TNF-α) concentrations. AT inflammation was characterized by accumulation of CD68(+) macrophages with a threefold increased gene expression of the macrophage markers CD68, EMR1, and CD14. Gene expression for cytokines IL-6, TNF-α, IL-8, and monocyte chemotactic protein-1 (MCP1) and for LPS-sensing CD14, toll-like receptor 4 (TLR4), translocating chain-associated membrane protein 2 was 2.5-5-fold higher in stromal cells of obese compared to lean. LPS-treated cultured stromal cells of obese women expressed a 5-16-fold stimulation of the same cytokines upregulated in vivo. Our data demonstrate that subclinical endotoxemia is associated with systemic and AT inflammation in obese pregnant women. Recognition of bacterial pathogens may contribute to the combined dysfunction of innate immunity and the metabolic systems in AT.
Authors:
Subhabrata Basu; Maricela Haghiac; Peter Surace; Jean-Claude Challier; Michele Guerre-Millo; Katherine Singh; Thaddeus Waters; Judi Minium; Larraine Presley; Patrick M Catalano; Sylvie Hauguel-de Mouzon
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-10-07
Journal Detail:
Title:  Obesity (Silver Spring, Md.)     Volume:  19     ISSN:  1930-739X     ISO Abbreviation:  Obesity (Silver Spring)     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-02-24     Completed Date:  2011-10-04     Revised Date:  2014-09-17    
Medline Journal Info:
Nlm Unique ID:  101264860     Medline TA:  Obesity (Silver Spring)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  476-82     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Adipose Tissue / immunology*,  metabolism
Adult
Antigens, CD / metabolism
C-Reactive Protein / metabolism
Chemokine CCL2 / metabolism
Cytokines / metabolism
Endotoxemia / etiology,  immunology*,  metabolism
Female
Humans
Immunity, Innate
Inflammation / etiology,  immunology*,  metabolism
Inflammation Mediators / metabolism*
Lipopolysaccharides / metabolism
Macrophages / metabolism
Membrane Glycoproteins / metabolism
Obesity / complications,  immunology*,  metabolism
Pregnancy
Pregnancy Complications / immunology*,  metabolism
Toll-Like Receptor 4 / metabolism
Young Adult
Grant Support
ID/Acronym/Agency:
HD022965/HD/NICHD NIH HHS; HD057236/HD/NICHD NIH HHS; R01 HD022965/HD/NICHD NIH HHS; UL1 RR024989/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD; 0/Chemokine CCL2; 0/Cytokines; 0/Inflammation Mediators; 0/Lipopolysaccharides; 0/Membrane Glycoproteins; 0/TRAM2 protein, human; 0/Toll-Like Receptor 4; 9007-41-4/C-Reactive Protein
Comments/Corrections

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