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Blood, 15 December 2001, Vol. 98, No. 13, pp. 3800-3808
PHAGOCYTES
High concentrations of lipopolysaccharide-binding protein in
serum of patients with severe sepsis or septic shock inhibit the
lipopolysaccharide response in human monocytes
Janine Zweigner,
Hans-Joachim Gramm,
Oliver C. Singer,
Karl Wegscheider, and
Ralf R. Schumann
From the Institut für Mikrobiologie und Hygiene,
Universitätsklinikum Charité, Medizinische Fakultät
der Humboldt-Universität zu Berlin, and Klinik für
Anaesthesiologie und operative Intensivmedizin,
Universitätsklinikum Benjamin Franklin, Freie Universität
Berlin, Germany, and the Institut für Statistik und
Ökonometrie, Universität Hamburg, Germany.
Lipopolysaccharide-binding protein (LBP), an
acute-phase protein recognizing lipopolysaccharide (LPS), catalyzes in
low concentrations its transfer to the cellular LPS receptor consisting
of CD14 and Toll-like receptor-4. It has recently been shown
that high concentrations of recombinant LBP can protect mice in a
peritonitis model from the lethal effects of LPS. To determine whether
in humans the acute-phase rise of LBP concentrations can inhibit LPS
binding to monocytes and induction of proinflammatory cytokines, LBP
concentrations were analyzed in 63 patients meeting the American
College of Chest Physicians/Society of Critical Care Medicine criteria
of severe sepsis or septic shock and the ability of these sera to
modulate LPS effects in vitro was assessed employing different assays. Transfer of fluorescein isothiocyanate-labeled LPS to human monocytes was assessed by a fluorescence-activated cell sorter-based method, and
activation of monocytes was investigated by measuring LPS-induced tumor
necrosis factor- secretion in the presence of the sera. Anti-LBP
antibodies and recombinant human LBP were instrumental for depletion
and reconstitution of acute-phase sera and subsequent assessment of
their modulating effects on LPS activity. Sera of patients with severe
sepsis/septic shock exhibited a diminished LPS transfer activity and
LPS-induced tumor necrosis factor- secretion as compared with sera
from healthy controls. LBP depletion of sepsis sera and addition of
rhLBP resulting in concentrations found in severe sepsis confirmed that
LBP was the major serum component responsible for the observed effects.
In summary, the inhibition of LPS effects by high concentrations of LBP
in acute-phase serum, as described here, may represent a novel defense
mechanism of the host in severe sepsis and during bacterial infections.
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