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L Szabo

Publications and source records attributed to L Szabo.

At least 55 records · Page 3Linked to original sources

Specific binding of endotoxin to human monocytes and mouse macrophages: serum requirement.

Specific binding of Bordetella pertussis and Neisseria meningitidis endotoxins to human monocytes and murine macrophages was demonstrated. Binding of B. pertussis endotoxin could be inhibited by endotoxins of Salmonella minnesota, Escherichia coli, and Klebsiella pneumoniae, the extent of inhibition being dependent on the origin of the lipopolysaccharides and on the origin of the mononuclear phagocytic cells. The binding of B. pertussis and N. meningitidis endotoxins which was mediated by the polysaccharide region of the endotoxins was serum dependent. The results indicated that the binding of endotoxin was promoted neither by natural antibodies directed against the endotoxin nor by proteins known to combine with endotoxins: immunoglobulins, albumin, or fibronectin; we have provided some evidence that complement components may play a role in the specific binding of endotoxins to the monocyte/macrophage membrane.

Animals↗

Structure of the terminal reducing heptasaccharide of polysaccharide 1 isolated from the Bordetella pertussis endotoxin.

The tetrasaccharide beta-D-glucopyranosyl-(1,3)-beta-D-glucopyranuronyl-(1, 2)-L-glycero-alpha-D-manno-heptopyranosyl-(1,5)-3-deoxy-D-manno-2- octulosonic acid was isolated after treatment of polysaccharide 1 of Bordetella pertussis endotoxin with nitrous acid. Taking into account previously identified di- and trisaccharide fragments and analytical data obtained for the intact polysaccharide 1, we present the structure of a heptasaccharide that is thought to represent the region immediately adjacent to the hydrophobic (lipid A) moiety of lipopolysaccharide 1 of the B. pertussis endotoxin. This heptasaccharide represents 50 to 60% of the complete polysaccharide structure.

Bordetella pertussis↗

Effect of sustained norepinephrine infusion on local cerebral blood flow in the rat.

In order to elucidate the possible role of noradrenergic hyperactivity in producing disturbances of cerebral circulation during hemorrhagic shock, the effect of prolonged norepinephrine infusion on local cerebral blood flow was studied in anesthetized and artificially ventilated rats. Intravenous infusion of 20 micrograms/(kg.min) norepinephrine for 2 hr produced circulatory shock characterized by progressive hypotension and acidosis. As a result, local cerebral blood flow, which was determined by autoradiography employing 14C-labeled iodoantipyrine in 79 different anatomical structures, decreased substantially in many areas. The most pronounced reductions were found in the regions supplied by the internal carotid artery, whereas the blood flow of the vertebral territory remained close to control. The blood supply of the cerebral cortex exhibited extreme heterogeneity with flow values below 0.10 ml/(min.gm). When either the intensity or the length of the infusion was reduced, no signs of circulatory breakdown could be observed. Variation of the infusion parameters demonstrated the dose-dependent nature of the cerebral blood flow response. Preinfusion blockade of alpha-receptors with 5 mg/kg phenoxybenzamine prevented the development of circulatory shock and reversed the decrease in cerebral blood flow induced by norepinephrine. The experimental results support the hypothesis that high concentration of norepinephrine in the vicinity of cerebral vessels produced by sympathetic hyperactivity might be an important factor in the etiology of blood flow deficiencies.

Acidosis↗

Isolation of a trisaccharide containing 2-amino-2-deoxy-D-galacturonic acid from the Bordetella pertussis endotoxin.

4-O-(2-Amino-2-deoxy-alpha-D-glucopyranosyl-6-O-(2-amino-2-deoxy-alpha-D-galactopyranuronyl)-D-glucopyranose, a branched-chain trisaccharide, was isolated after hydrolysis of Bordetella pertussis endotoxin with 4 M HCl for 1 h at 100 degrees C. The trisaccharide was present in both polysaccharide moieties of the two constituent lipopolysaccharides of this endotoxin. Its structure was established by analysis of the 400-MHz nuclear magnetic resonance spectrum and by chemical and enzymatic degradation.

Bordetella pertussis↗