Abstract
LPS-binding protein (LBP) and CD14 potentiate cell activation by LPS, contributing to lethal endotoxemia. We analyzed the contribution of LBP/CD14 in models of bacterial infection. Mice pretreated with mAbs neutralizing CD14 or LBP showed a delay in TNF-alpha production and died of overwhelming infection within 24 h, after a challenge with 250 CFU of virulent Klebsiella pneumoniae. Blockade of TNF-alpha also increased lethality, whereas pretreatment with TNF-alpha protected mice, even in the presence of LBP and CD14 blockade. Anti-LBP or anti-CD14 mAbs did not improve or decrease lethality with a higher inoculum (10(5) K. pneumoniae) and did not affect outcome following injections of low or high inocula of Escherichia coli O111. These results point to the essential role of LBP/CD14 in innate immunity against virulent bacteria.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acute-Phase Proteins*
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Animals
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Antibodies, Monoclonal
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Bacteremia / etiology
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Bacteremia / immunology
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Carrier Proteins / antagonists & inhibitors
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Carrier Proteins / immunology*
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Carrier Proteins / metabolism*
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Endotoxemia / immunology
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Escherichia coli / immunology
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Escherichia coli / pathogenicity
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Female
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Gram-Negative Bacteria / immunology*
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Gram-Negative Bacteria / pathogenicity
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Gram-Negative Bacterial Infections / etiology
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Gram-Negative Bacterial Infections / immunology
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Klebsiella pneumoniae / immunology
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Klebsiella pneumoniae / pathogenicity
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Lipopolysaccharide Receptors / metabolism*
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Lipopolysaccharides / metabolism*
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Lipopolysaccharides / toxicity
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Membrane Glycoproteins*
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Mice
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Neutralization Tests
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Neutrophils / immunology
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Sepsis / etiology
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Sepsis / immunology
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Tumor Necrosis Factor-alpha / biosynthesis
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Tumor Necrosis Factor-alpha / pharmacology
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Virulence
Substances
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Acute-Phase Proteins
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Antibodies, Monoclonal
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Carrier Proteins
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Lipopolysaccharide Receptors
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Lipopolysaccharides
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Membrane Glycoproteins
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Tumor Necrosis Factor-alpha
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lipopolysaccharide-binding protein