Lipopolysaccharide-binding protein: a possible diagnostic marker for Gram-negative bacteremia in neutropenic cancer patients

2003 ◽  
Vol 29 (12) ◽  
pp. 2157-2161 ◽  
Author(s):  
Claudi S. M. Oude Nijhuis ◽  
Edo Vellenga ◽  
Simon M. G. J. Daenen ◽  
Winette T. A. van der Graaf ◽  
Jourik A. Gietema ◽  
...  
2009 ◽  
Vol 55 (2) ◽  
pp. 295-304 ◽  
Author(s):  
Tanja Vollmer ◽  
Cornelia Piper ◽  
Knut Kleesiek ◽  
Jens Dreier

Abstract Background: Infectious endocarditis (IE) is a bacterial infection of the endocardium. Diagnosis is based on results obtained from echocardiography, blood cultures, and molecular genetic screening for bacteria and on data for inflammatory markers such as the leukocyte (WBC) count and the C-reactive protein (CRP) concentration. The aim of the present study was to evaluate lipopolysaccharide-binding protein (LBP) as a supportive biomarker for the diagnosis and therapeutic monitoring of IE. Methods: We measured LBP and CRP concentrations and WBC counts in 57 IE patients at hospital admission, 40 patients with noninfectious heart valve diseases (HVDs), and 55 healthy blood donors. The progression of these 3 markers and the influence of cardiac surgery on them were evaluated in 29 IE patients and 21 control patients. Results: Serum LBP concentrations were significantly higher in IE patients [mean (SD), 33.41 (32.10) mg/L] compared with HVD patients [6.67 (1.82) mg/L, P < 0.0001] and healthy control individuals [5.61 (1.20) mg/L]. The progression in the LBP concentration during therapy of IE patients correlated with the changes in the CRP concentration. The 2 markers were equally influenced by antibiotic treatment and surgical intervention. Conclusions: Serial LBP measurement may provide an effective and useful tool for evaluating the response to therapy in IE patients. We found a strong correlation between LBP and CRP concentrations; LBP has a tendency to increase earlier in cases of reinfection.


2011 ◽  
Vol 39 (4) ◽  
pp. 989-993 ◽  
Author(s):  
Ralf R. Schumann

LBP [LPS (lipopolysaccharide)-binding protein] was discovered approximately 25 years ago. Since then, substantial progress has been made towards our understanding of its function in health and disease. Furthermore, the discovery of a large protein family sharing functional and structural attributes has helped in our knowledge. Still, key questions are unresolved, and here an overview on the old and new findings on LBP is given. LBP is an acute-phase protein of the liver, but is also synthesized in other cells of the organism. While LBP is named after the ability to bind to LPS of Gram-negative bacteria, it also can recognize other bacterial compounds, such as lipopeptides. It has been shown that LBP is needed to combat infections; however, the main mechanism of action is still not clear. New findings on natural genetic variations of LBP leading to functional consequences may help in further elucidating the mechanism of LBP and its role in innate immunity and disease.


2001 ◽  
Vol 18 (Supplement 21) ◽  
pp. 119-120
Author(s):  
A. Nierhaus ◽  
B. Montag ◽  
D. Frings ◽  
N. Suerhoff ◽  
J. Schulte am Esch

2001 ◽  
Vol 167 (5) ◽  
pp. 2759-2765 ◽  
Author(s):  
Didier Le Roy ◽  
Franco Di Padova ◽  
Yoshiyuki Adachi ◽  
Michel Pierre Glauser ◽  
Thierry Calandra ◽  
...  

Blood ◽  
2008 ◽  
Vol 111 (4) ◽  
pp. 2462-2469 ◽  
Author(s):  
Jason W. Chien ◽  
Michael J. Boeckh ◽  
John A. Hansen ◽  
Joan G. Clark

Lipopolysaccharide binding protein (LBP) function is dependent on circulating LBP levels. Disturbance of LBP transcription regulation may influence the risk for clinical events. In a nested case-control study using a single nucleotide polymorphism haplotype tagging (tagSNP) approach, we assessed whether genetic variation in the LBP gene influences the risk for Gram-negative (GN) bacteremia after allogeneic hematopoietic cell transplantation (HCT), then validated the association in a prospective cohort by correlating genetic variation with basal serum LBP levels and mortality. Presence of the tagSNP 6878 C allele among patients was associated with a 2-fold higher risk for GN bacteremia (odds ratio = 2.15; 95% confidence interval [CI], 1.31-3.52, P = .002). TagSNP 6878 was in strong linkage disequilibrium with 3 SNPs in the LBP promoter, one of which was SNP 1683 (r2 = 0.8), located in a CAAT box that regulates LBP promoter efficiency. SNP 1683 was associated with higher median basal serum LBP levels (TT 8.07 μg/mL; TC 10.40 μg/mL; CC 17.39 μg/mL; P = .002), and a 5-fold increase in GN bacteremia related mortality after HCT (hazard ratio = 4.83; 95% CI, 1.38-16.75, P = .013). These data suggest that transcriptional regulation of the LBP gene contributes to the risk for developing GN bacteremia and death after HCT.


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