Lipopolysaccharide-binding molecules: transporters, blockers and sensors

Chaby, Richard

doi:10.1007/s00018-004-4020-4

Cited by 71 publications

(56 citation statements)

References 169 publications

(133 reference statements)

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“…In this context, PLTP operates in close cooperation with the scavenging properties of lipoprotein acceptors that have been previously recognized as key vehicles in LPS transport (19,22,23,30,57). Increasing the circulating level of PLTP arises here as a new and promising strategy in preventing endotoxic shock.…”

Section: Discussionmentioning

confidence: 99%

Effect of Plasma Phospholipid Transfer Protein Deficiency on Lethal Endotoxemia in Mice

Gautier

Klein

Deckert

et al. 2008

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Effect of Plasma Phospholipid Transfer Protein Deficiency on Lethal Endotoxemia in Mice

Gautier

Klein

Deckert

et al. 2008

Journal of Biological Chemistry

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“…A number of cationic antimicrobial peptides and proteins are able to bind the endotoxin LPS and modulate the cell inflammatory response induced by the endotoxin LPS (49). Some molecules like BPI (bactericidal/permeability-increasing protein), granulysin/NK lysin, histatins, histone H2A, LL-37, and SLPI can neutralize the pro-inflammatory effects of LPS, whereas another molecule like azurocidin/HBP (heparin-binding protein) can enhance the capacity of LPS to induce the release of pro-inflammatory mediators by cells.…”

Section: Discussionmentioning

confidence: 99%

Elafin, an Elastase-specific Inhibitor, Is Cleaved by Its Cognate Enzyme Neutrophil Elastase in Sputum from Individuals with Cystic Fibrosis

Guyot

Butler

McNally

et al. 2008

Journal of Biological Chemistry

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Elafin is a neutrophil serine protease inhibitor expressed in lung and displaying anti-inflammatory and anti-bacterial properties. Previous studies demonstrated that some innate host defense molecules of the cystic fibrosis (CF) and chronic obstructive pulmonary disease airways are impaired due to increased proteolytic degradation observed during lung inflammation. In light of these findings, we thus focused on the status of elafin in CF lung. We showed in the present study that elafin is cleaved in sputum from individuals with CF. Pseudomonas aeruginosa-positive CF sputum, which was found to contain lower elafin levels and higher neutrophil elastase (NE) activity compared with P. aeruginosa-negative samples, was particularly effective in cleaving recombinant elafin. NE plays a pivotal role in the process as only NE inhibitors are able to inhibit elafin degradation. Further in vitro studies demonstrated that incubation of recombinant elafin with excess of NE leads to the rapid cleavage of the inhibitor. Two cleavage sites were identified at the N-terminal extremity of elafin (Val-5-Lys-6 and Val-9 -Ser-10). Interestingly, purified fragments of the inhibitor (Lys-6 -Gln-57 and Ser-10 -Gln-57) were shown to still be active for inhibiting NE. However, NE in excess was shown to strongly diminish the ability of elafin to bind lipopolysaccharide (LPS) and its capacity to be immobilized by transglutamination. In conclusion, this study provides evidence that elafin is cleaved by its cognate enzyme NE present at excessive concentration in CF sputum and that P. aeruginosa infection promotes this effect. Such cleavage may have repercussions on the innate immune function of elafin.

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“…Lipopolysaccharide, as an amphiphilic molecule in biological fluids, is always bound to other molecules such as peptides and proteins. 41 It is well recognized that human plasma neutralizes lipopolysaccharide up to 6 µg/ml 42 and that lipopolysaccharide diluted in plasma before application is less effective than lipopolysaccharide diluted in crystalloid solution.…”

Section: Discussionmentioning

confidence: 99%

The NFKB1 Promoter Polymorphism (−94ins/delATTG) Alters Nuclear Translocation of NF-κB1 in Monocytes after Lipopolysaccharide Stimulation and Is Associated with Increased Mortality in Sepsis

Adamzik

Schäfer²,

Frey

et al. 2013

Anesthesiology

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Background: Because the nuclear factor-κB (NF-κB) coupled pathway is believed to amplify inflammation prevailing in sepsis, the authors tested the hypotheses that the insertiondeletion polymorphism (−94ins/delATTG) (1) alters nuclear translocation of nuclear factor-κB and activator protein-1 (NF-κB1) in monocytes after lipopolysaccharide stimulation; (2) affects lipopolysaccharide-induced NF-κB1 messenger RNA expression, tumor necrosis factor α concentrations, and tissue factor activity; and (3) may be associated with increased 30-day mortality in patients with sepsis. Methods: Nuclear translocation of NF-κB1 in monocytes after lipopolysaccharide stimulation from healthy blood donors was performed with immunofluorescence staining (n = 5 each). Lipopolysaccharide-induced NF-κB1 messenger RNA expression was measured with real-time polymerase chain reaction (PCR; n = 60), tumor necrosis factor α concentrations with a multiplexing system kit (n = 60), and tissue factor activity with thromboelastometry (n = 105). In a prospective study, multivariate proportional hazard analysis tested 30-day mortality in patients with sepsis (n = 143). Methods and Results:The homozygous deletion genotype compared with the homozygous insertion genotype was associated with a nearly twofold increase in nuclear translocation of NF-κB1 (P = 0.001), a threefold difference in NF-κB1 What We Already Know about This Topic• The nuclear factor-κB and activator protein-1-coupled signaling pathway of the innate immune system is known to amplify and perpetuate inflammatory and coagulatory mechanisms in sepsis• Genetic variations that alter nuclear factor-κB gene expression could affect pathophysiologic mechanisms and thereby influence mortality in severe sepsis What This Article Tells Us That Is New• A functional insertion-deletion polymorphism in the promoter of nuclear factor-κB and activator protein-1 affected expression and regulation of mediators of inflammation and coagulation in vitro • Expression of the same polymorphism was associated with increased 30-day mortality in patients with severe sepsis Downloaded from anesthesiology.pubs.asahq.org by guest on 06/07/2019

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Lipopolysaccharide-binding molecules: transporters, blockers and sensors

Cited by 71 publications

References 169 publications

Effect of Plasma Phospholipid Transfer Protein Deficiency on Lethal Endotoxemia in Mice

Effect of Plasma Phospholipid Transfer Protein Deficiency on Lethal Endotoxemia in Mice

Elafin, an Elastase-specific Inhibitor, Is Cleaved by Its Cognate Enzyme Neutrophil Elastase in Sputum from Individuals with Cystic Fibrosis

The NFKB1 Promoter Polymorphism (−94ins/delATTG) Alters Nuclear Translocation of NF-κB1 in Monocytes after Lipopolysaccharide Stimulation and Is Associated with Increased Mortality in Sepsis

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