Document Detail

Systemic inflammation increases intestinal permeability during experimental human endotoxemia.
MedLine Citation:
PMID:  19295480     Owner:  NLM     Status:  MEDLINE    
Although the gut is often considered the motor of sepsis, the relation between systemic inflammation and intestinal permeability in humans is not clear. We analyzed intestinal permeability during experimental endotoxemia in humans. Before and during experimental endotoxemia (Escherichia coli LPS, 2 ng/kg), using polyethylene glycol (PEG) as a permeability marker, intestinal permeability was analyzed in 14 healthy subjects. Enterocyte damage was determined by intestinal fatty acid binding protein. Endotoxemia induced an inflammatory response. Urinary PEGs 1,500 and 4,000 recovery increased from 38.8 +/- 6.3 to 63.1 +/- 12.5 and from 0.58 +/- 0.31 to 3.11 +/- 0.93 mg, respectively (P < 0.05). Intestinal fatty acid binding protein excretion was not affected by endotoxemia. The peak serum IL-10 concentrations correlated with the increase in PEG 1,500 recovery (r = 0.48, P = 0.027). Systemic inflammation results in an increased intestinal permeability. The increase in intestinal permeability is most likely caused by inflammation-induced paracellular permeability, rather than ischemia-mediated enterocyte damage.
Falco Hietbrink; Marc G H Besselink; Willem Renooij; Martin B M de Smet; Annelies Draisma; Hans van der Hoeven; Peter Pickkers
Publication Detail:
Type:  Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Shock (Augusta, Ga.)     Volume:  32     ISSN:  1540-0514     ISO Abbreviation:  Shock     Publication Date:  2009 Oct 
Date Detail:
Created Date:  2009-09-16     Completed Date:  2010-01-14     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9421564     Medline TA:  Shock     Country:  United States    
Other Details:
Languages:  eng     Pagination:  374-8     Citation Subset:  IM    
Department of Surgery, University Medical Center Utrecht, Utrecht, The Netherlands.
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MeSH Terms
Endotoxemia / chemically induced,  metabolism*,  pathology*
Fatty Acid-Binding Proteins / metabolism
Interleukin-10 / blood
Intestines / metabolism*,  pathology*
Lipopolysaccharides / toxicity
Polyethylene Glycols / metabolism
Systemic Inflammatory Response Syndrome / metabolism,  physiopathology*
Young Adult
Reg. No./Substance:
0/FABP2 protein, human; 0/Fatty Acid-Binding Proteins; 0/Lipopolysaccharides; 0/Polyethylene Glycols; 130068-27-8/Interleukin-10

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