Lipopolysaccharide-binding protein

The genes coding for CETP and PLTP belong to one gene family, which also includes lipopolysaccharide-binding-protein (LBP) and bactericidal/permeability-increasing-protein (BPI). This common descent not only becomes clear from a considerable sequence similarity (45-65% homology at the cDNA level), but also from substantial conservation of exon/intron transitions. 

Qureshi, N., Perera, P.-Y., Shen, J., Zhang, G., Lenschat, A., Splitter G., Morrison, D.C., and Vogel, S.N. (2003) The proteasome as a lipopolysaccharide-binding protein in macrophages Differential effects of proteasome inhibition on lipopolysaccharide-induced signaling events. J. Immunol. 171, 1515. 

Gutsmann, T., Schromm, A.B., Koch, M.H.J., Kusumoto, S., Fukase, K., Oikawa, M., Seydel, U., Brandenburg, K. Lipopolysaccharide-binding protein-mediated interaction of lipid A from different origin with phospholipid membranes. Phys Chem Chem Phys 2 (2000) 4521—4528. 

Tobias, P.S., Soldau, K., Gegner, J.A., Mintz, D., Ulevitch, R.J. Lipopolysaccharide binding protein-mediated complexation of lipopolysaccharide with soluble CD 14. J Biol Chem. 270 (1995) 10482-10488. 

Zweigner, J., Gramm, H.J., Singer, O.C., Wegscheider, K., Schumann, R.R. High concentrations of lipopolysaccharide-binding protein in serum of patients with severe sepsis or septic shock inhibit the lipopolysaccharide response in human monocytes. Blood 2001, 98 (2001) 3800-3808. 

Weersink, A.J.L., van Kessel, K.P.M., van den Tol, M.E., van Strijp, J.A.G., Torensma, R., Verhoef, J., Elsbach, R, Weiss, J. Human granulocytes express a 55 kDa lipopolysaccharide-binding protein on the cell surface that is identical to the bactericidal/permeability-increasing protein. J Immunol 150 (1992) 253-263. 

Calvano, S.E., Thompson, W.A., Marra, M.N., Coyle, S.M., de Riesthal, H.F., Trousdale, R.K., Barie, P.S., Scott, R.W., Moldawer, L.L., Lowry, S.F. Changes in polymorphonuclear leukocyte surface and plasma bactericidal/permeability-increasing protein and plasma lipopolysaccharide binding protein during endotoxemia or sepsis. Arch Surg 129 (1994) 220-226. 

Schumann RR, Leong SR, Flaggs GW, Gray PW, Wright SD, et al. 1990. Structure and function of lipopolysaccharide binding protein. Science 249 1429-31... 

De Haas CJ. New insights into the role of serum amyloid P component, a novel lipopolysaccharide-binding protein. FEMS Immunol Med Microbiol 1999 26 197-202. 

Schumann RR, Kirschning CJ, Unebehaun A, et al. The lipopolysaccharide-binding protein is a secretory class 1 acute-phase protein whose gene is transcriptionally activated by aprf/stat/3 and other cytokine-inducible nuclear proteins. Mol Cell Biol 1996 16 3490-3503. 

Pugin J, Shurer-Maly C-C, Leturcq D, Moriarty A, Ulevitch RJ, Tobias PS. Lipo-polysaccharide activation of human endothelial and epithelial cells is mediated by lipopolysaccharide-binding protein and soluble CD14. Proc Natl Acad Sci USA 1993 90 2744-2748. 

Recently, PHB beads for endotoxin removal were developed by fusing the human lipopolysaccharide binding protein (hLBP) to PhaP immobilized in vitro on PHB particles via the natural hydrophobic interaction between PhaP and PHB [71]. 

Endotoxin removing method based on lipopolysaccharide binding protein and polyhydroxyalkanoate binding protein PhaP. Biomacromolecules, 12, 602 -608. 

The peptide-induced inhibition of the intercalation of lipid A into liposomes made from phosphatidylserine (PS) alone or mediated by lipopolysaccharide-binding protein (LBP), was determined by FRET spectroscopy applied as a probe dilution assay (4). First the peptide, then lipid A, followed by LBP (or vice versa) were added to the liposomes, which were labelled with the donor dye NBD-phosphatidylethanolamine (NBD-PE) and acceptor dye Rhodamine-PE. The final concentrations were peptide and lipid 1 pM and LBP 0.1 pM. Intercalation was monitored as the increase of the ratio of the donor intensity Id at 531 nm to that of the acceptor intensity U at 593 nm (FRET signal) with on time. 

The interaction of lipid A with Pcplalf was studied with (a) FTIR by monitoring the gel to liquid crystalline phase transition of the acyl chains of lipid A, (b) SAXS by analyzing the aggregate structure of lipid A, and (c) FRET by investigating the potential peptide-mediated inhibition of the intercalation of lipid A into model liposomes, induced by lipopolysaccharide binding protein (LBP). 

Wurfel, M. M., and Wright, S. D. (1997). Lipopolysaccharide-binding protein and soluble CD14 transfer lipopolysaccharide to phospholipid bilayers. J. Immunol. 158, 3925-3934. 

Jack, R.S., Fan, X., Bernheiden, M., Rune, G., Ehlers, M., Weber, A., Kirsch, G., Mentel, R., Furll, B., Freudenberg, M., Schmitz, G., Stelter and Schiitt, C. (19 Lipopolysaccharide-binding protein is required to combat a murine Gram-negative bacterial infection. Nature 389, 742-745. 

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