The Experts below are selected from a list of 195 Experts worldwide ranked by ideXlab platform
Nobuhiro Yuki - One of the best experts on this subject based on the ideXlab platform.
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molecular mimicry between gangliosides and Lipopolysaccharides of campylobacter jejuni isolated from patients with guillain barre syndrome and miller fisher syndrome
The Journal of Infectious Diseases, 1997Co-Authors: Nobuhiro YukiAbstract:Some patients developed Guillain-Barre syndrome (GBS) after being given bovine gangliosides. Patients with GBS subsequent to Campylobacter jejuni enteritis frequently have IgG antibody to GM 1 ganglioside. Miller Fisher syndrome (MFS), a variant of GBS, is associated with IgG antibody to GQ 1b ganglioside. The existence of molecular mimicry between GM 1 and lipopolysaccharide of C. jejuni isolated from a GBS patient and that between GQ 1b and C. jejuni Lipopolysaccharides from patients with MFS are shown herein. The molecular mimicry between infectious agents and gangliosides may function in the production of anti-ganglioside antibodies and the development of GBS and MFS.
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molecular mimicry between gq1b ganglioside and Lipopolysaccharides of campylobacter jejuni isolated from patients with fisher s syndrome
Annals of Neurology, 1994Co-Authors: Nobuhiro Yuki, Kahiko Saito, H. Yoshino, Takao Taki, Shizuo Handa, Masaki Takahashi, Tadashi MiyatakeAbstract:We isolated Campylobacter jejuni from 2 patients with Fisher's syndrome subsequent to enteritis. Crude lipopolysaccharide fractions were extracted from the bacteria and separated by thin-layer chromatography. Monoclonal antibodies to GQ1b ganglioside (GMR 13 and 7F5) reacted with both lipopolysaccharide fractions, indicating that the Lipopolysaccharides bear the GQ1b epitope. This is the first report of molecular mimicry between neural tissue components and the antecedent infectious agents of Fisher's syndrome.
Thomas W. Stief - One of the best experts on this subject based on the ideXlab platform.
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Coagulation Activation by Lipopolysaccharides
Clinical and Applied Thrombosis-Hemostasis, 2007Co-Authors: Thomas W. StiefAbstract:Lipopolysaccharides at approximate plasma reactivities >3 ng/mL or β-glucans at >0.5-1 μg/mL are toxic for human blood; lipopolysaccharide interacts with membrane components of susceptible cells (eg, monocytes) activating phospholipase A2 that destroys the cell membrane. Cell fragments (microparticles or DNA) possess polynegative niches that activate intrinsic hemostasis. Pathologic disseminated intravascular coagulation arises. Blood vessels are obstructed by disseminated thrombi, and vital organ areas become ischemic. Multiorgan failure threatens life of the patient. Diagnosis and therapy of pathologic disseminated intravascular coagulation is of extreme clinical importance. For early diagnosis of pathologic disseminated intravascular coagulation, specific activation markers of coagulation (eg, plasmatic amidolytic thrombin activity) or the plasmatic lipopolysaccharide or glucan reactivity can be measured. A new treatment target might be kallikrein or factor XIIa; 10 to 20 mM arginine is the approximate...
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Coagulation Activation by Lipopolysaccharides
Clinical and applied thrombosis hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis Hemostasis, 2007Co-Authors: Thomas W. StiefAbstract:Lipopolysaccharides at approximate plasma reactivities >3 ng/mL or β-glucans at >0.5-1 μg/mL are toxic for human blood; lipopolysaccharide interacts with membrane components of susceptible cells (e...
Tadashi Miyatake - One of the best experts on this subject based on the ideXlab platform.
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molecular mimicry between gq1b ganglioside and Lipopolysaccharides of campylobacter jejuni isolated from patients with fisher s syndrome
Annals of Neurology, 1994Co-Authors: Nobuhiro Yuki, Kahiko Saito, H. Yoshino, Takao Taki, Shizuo Handa, Masaki Takahashi, Tadashi MiyatakeAbstract:We isolated Campylobacter jejuni from 2 patients with Fisher's syndrome subsequent to enteritis. Crude lipopolysaccharide fractions were extracted from the bacteria and separated by thin-layer chromatography. Monoclonal antibodies to GQ1b ganglioside (GMR 13 and 7F5) reacted with both lipopolysaccharide fractions, indicating that the Lipopolysaccharides bear the GQ1b epitope. This is the first report of molecular mimicry between neural tissue components and the antecedent infectious agents of Fisher's syndrome.
Robert S Munford - One of the best experts on this subject based on the ideXlab platform.
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lipopolysaccharide binding protein and phospholipid transfer protein release Lipopolysaccharides from gram negative bacterial membranes
Infection and Immunity, 2000Co-Authors: C J Vesy, G Wolfbauer, J J Albers, Richard L. Kitchens, Robert S MunfordAbstract:Although animals mobilize their innate defenses against gram-negative bacteria when they sense the lipid A moiety of bacterial lipopolysaccharide (LPS), excessive responses to this conserved bacterial molecule can be harmful. Of the known ways for decreasing the stimulatory potency of LPS in blood, the binding and neutralization of LPS by plasma lipoproteins is most prominent. The mechanisms by which host lipoproteins take up the native LPS that is found in bacterial membranes are poorly understood, however, since almost all studies of host-LPS interactions have used purified LPS aggregates. Using native Salmonella enterica serovar Typhimurium outer membrane fragments (blebs) that contained 3H-labeled lipopolysaccharide (LPS) and 35S-labeled protein, we found that two human plasma proteins, LPS-binding protein (LBP) and phospholipid transfer protein (PLTP), can extract [3H]LPS from bacterial membranes and transfer it to human high-density lipoproteins (HDL). Soluble CD14 (sCD14) did not release LPS from blebs yet could facilitate LBP-mediated LPS transfer to HDL. LBP, but not PLTP, also promoted the activation of human monocytes by bleb-derived LPS. Whereas depleting or neutralizing LBP significantly reduced LPS transfer from blebs to lipoproteins in normal human serum, neutralizing serum PLTP had no demonstrable effect. Of the known lipid transfer proteins, LBP is thus most able to transfer LPS from bacterial membranes to the lipoproteins in normal human serum.
J L Penner - One of the best experts on this subject based on the ideXlab platform.
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Lipopolysaccharides of campylobacter jejuni serotype o 19 structures of core oligosaccharide regions from the serostrain and two bacterial isolates from patients with the guillain barre syndrome
Biochemistry, 1994Co-Authors: Gerald O Aspinall, Armando G Mcdonald, Henrianna Pang, Linda A Kurjanczyk, J L PennerAbstract:Lipopolysaccharides from phenol-water extraction of cells of Campylobacter jejuni serotype O:19 were separated into a water-soluble gel of low M(r) and a water-soluble component of high M(r). Acetic acid hydrolysis of the ketosidic linkages to lipid A furnished respectively a core oligosaccharide, the structure of which is reported herein, and an O antigenic polysaccharide. Structural investigations were performed on the O-deacetylated lipopolysaccharide of low M(r), the liberated core oligosaccharide and the various products from removal of neuraminic acid and phosphate residues, and from the Smith degradation. It is concluded that the lipopolysaccharide from the serostrain has a core region with two types of closely related oligosaccharide chains showing striking homologies with gangliosides, the first with a single N-acetylneuraminic acid residue in an outer chain resembling GM1 and the second with two N-acetyl-neuraminic acid residues with a terminal region resembling GD1a. Similar experiments were carried out on Lipopolysaccharides of low M(r) from bacterial isolates OH 4384 and OH 4382 serotyped as O:19 that had been obtained from two patients who subsequently developed the Guillain-Barre syndrome. The core oligosaccharide region of lipopolysaccharide from the former isolate differed only slightly from that of the serostrain, whereas that from the latter isolate was distinctly shorter.