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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Shigella sonnei phase I and phase II lipopolysaccharides were examined using passive hemagglutination, immunodiffusion and immunoelectrophoresis. Moreover, O-antigen preparations of phase I obtained by three different methods were separated in SDS polyacrylamide gel electrophoresis into two fractions: L1 and L2, whereas phase II lipopolysaccharide showed one fraction (LI) only. The results of the serological investigations of three mentioned above preparations indicate that the heterogeneity of phase I O-antigen is natural, and not caused by extraction procedures. Shigella sonnei phase I cells produce two types of lipopolysaccharide molecules: I) with core regions substituted by phase I-specific polysaccharide chains, and 2) with core regions unsubstituted, having phase II specificity.
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PMID:Heterogeneity of Shigella sonnei phase I O-antigen. 618 56

An enzyme-linked immunosorbent assay (ELISA) was developed for determination of the IgA, IgM and IgG antibody responses against a lipopolysaccharide antigen representing Shigella sonnei phase I bacteria. Two or more sera from 33 patients infected with Shigella sonnei were collected during a 12 month period after onset of the disease. Convalescent sera from 56 patients with other enteric infections (salmonellosis, yersiniosis, campylobacteriosis) and sera drawn from 40 healthy blood donors served as controls. Twenty-eight of the 33 patients (85%) had at least one serum specimen where two or three of the immunoglobulin titres were classified as positive (greater than + 2SD above mean titres seen in healthy blood donors), whereas only ten of 56 patients (18%) with other enteric infections had similarly elevated titres (p less than 0.001). The Shigella sonnei ELISA using purified lipopolysaccharide as antigen is considered more sensitive and specific than the formerly used agglutination tests.
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PMID:Antibody response to Shigella sonnei infection determined by an enzyme-linked immunosorbent assay. 634 88

Shigella sonnei lipopolysaccharide (LPS) was injected intravenous (iv) or into the lateral cerebral ventricle (icv) of freely moving rats. Iv injection of 320 micrograms/Kg reduced arterial blood pressure, increased heart rate and did not change pressor response and reflex bradycardia induced by iv bolus injection of phenylephrine (5 micrograms/Kg). Iv injection of 640 micrograms/Kg reduced arterial blood pressure and heart rate, and altered baroreceptor reflexes. Icv injection of LPS (up to 50 micrograms/rat) neither changed resting blood pressure and heart rate nor modified phenylephrine induced pressor response and reflex bradycardia. Results suggest that S. sonnei endotoxin determines cardiovascular changes mainly through baroreceptor resetting. Data also seem to rule out a central nervous system involvement.
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PMID:Cardiovascular responses of conscious rats to acute intravenous and intracerebroventricular administration of Shigella sonnei endotoxin. 636 36

The form-1 antigen of Shigella sonnei was transferred to the avirulent Salmonella typhi strain 21a and the resulting 5076-1C transconjugate strain was tested for safety and immunogenicity as a candidate oral vaccine. The transconjugant strain was shown to be well tolerated and safe in 19 human volunteers who were fed from 1 X 10(7) to 1 X 10(10) organisms. Only two of 10 volunteers tested had developed a rise in antibody titer to the lipopolysaccharide of the hybrid 5076-1C strain.
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PMID:Safety and antigenicity of typhoid-Shigella sonnei vaccine (strain 5076-1C). 636 77

Salmonella typhi 5076-1C, a potential live, oral vaccine for protection against typhoid fever and Shigella sonnei shigellosis, expresses the S. sonnei form I antigen and normal S. typhi somatic antigens. Polysaccharide antigens of this galactose epimeraseless genetic derivative strain were hot phenol-water extracted from cells grown with (+gal) and without (-gal) galactose. Ultracentrifugation of the aqueous layer from (+gal) cells resulted in a lipopolysaccharide (LPS) pellet having core-linked S. typhi O-antigen but no core-linked form I antigen; the LPS from (-gal) cells lacked O-antigen. The form I antigen, obtained from the supernatant, was purified by alcohol precipitation and ion exchange chromatography. Unlinked form I and S. typhi O-polysaccharide antigens, both present in the (+gal) supernatant, were further separated by gel filtration. Chemical analyses revealed the 5076-1C form I antigen to be a polymer (Mr = 14,000-20,000) having O-disaccharide repeating units comprised of 2-acetamido-4-amino-2, 4,6-trideoxy-D-galactose and 2-acetamido-2-deoxy-L-altruronic acid. Unlike parental S. sonnei form I LPS, the 5076-1C form I antigen lacked core lipid A, had low phosphorus content, and migrated in polyacrylamide gels with lower relative mobility. In contrast to current concepts of LPS assembly, these data indicate that 5076-1C form I antigen is transported to the cell surface without covalent linkage to core lipid A, and exists as a polymerized, antigenic surface entity.
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PMID:Unusual lipopolysaccharide antigens of a Salmonella typhi oral vaccine strain expressing the Shigella sonnei form I antigen. 637 5

Monoclonal antibodies directed against O-specific antigens of Vibrio cholerae O1 lipopolysaccharide were used in two different enzyme-linked immunosorbent assays (ELISAs), designed for identification and serotyping of V. cholerae O1. In the sandwich ELISA, a monoclonal antibody against the group-specific antigen was used as capture antibody, whereas peroxidase-conjugated monoclonal antibodies directed against group- and type-specific antigens were used as the second antibodies. Monoclonal antibodies were also used in ELISA inhibition tests with whole bacteria as inhibitors in microtiter trays coated with V. cholerae O1 lipopolysaccharide. In addition, the monoclonal antibodies were shown to be useful in slide agglutination tests. The enzyme immunoassays were equally sensitive, showing positive reactions with all V. cholerae O1 strains tested, whereas all V. cholerae non-O1 as well as strains of Escherichia coli, Shigella sonnei, Salmonella spp., Citrobacter freundii, and Brucella abortus were negative. The microtiter application makes the immunoassays suitable with low consumption of reagents for screening of samples from suspected cases as well as from the environment.
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PMID:Monoclonal antibody-based enzyme-linked immunosorbent assays for identification and serotyping of Vibrio cholerae O1. 639 21

Shigella sonnei lipopolysaccharide (LPS), either in phase I (extracted from the smooth strains), or in phase II (extracted from the rough strains) reduced mean arterial pressure and heart rate following a 640 micrograms/Kg intravenous (iv) bolus injection in the urethane-anesthetized rat. Lower doses were without significant effects. Escherichia coli LPS (640 micrograms/Kg iv) produced a greater and more prolonged hypotension, however the negative chronotropic effect was less severe. The iv injection of the lipid A moiety of the LPS molecule of Shigella sonnei resulted in a more pronounced hypotensive effect than that obtained with the parent LPS, thus showing that lipid A is the vasodilatating fraction of the molecule. When lipid A was injected in rats pretreated with aspirin or with naloxone, the hypotensive effect was significantly reduced and the decrease in heart rate was reverted in tachycardia. In atropine-pretreated, surgically bivagotomized rats, iv injection of lipid A was followed by a long-lasting pressor effect. The date indicate that Shigella sonnei endotoxin has cardiovascular effects, mainly due to its lipid A moiety of the molecule. The hypotensive effect involves a wide range of mechanisms.
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PMID:Cardiovascular effects of Shigella sonnei endotoxin in the rat. 676 10

Escherichia coli O127:B8 lipopolysaccharide (LPS) inhibited oxygen consumption by isolated mouse liver mitochondria at 10 micrograms of LPS per mg of protein when glutamate + malate was the substrate and adenosine 5'-diphosphate had been added (state 3 respiration), but had little effect when adenosine 5'-diphosphate was not added (state 4 respiration). LPS stimulated state 4 respiration at 10 micrograms/mg of mitochondrial protein when succinate was the substrate but had little effect on state 3 respiration. Lipid A from Shigella sonnei at 2 micrograms/mg of mitochondrial protein also stimulated state 4 respiration but did not affect state 3 respiration with succinate as the substrate. Lipid A, unlike LPS, caused a decrease in the adenosine 5'-diphosphate/O ratio. LPS at 100 micrograms/mg of mitochondrial protein impaired the reduction of cytochromes aa3, c, and b when succinate was the substrate but not when reduced nicotinamide dinucleotide, dithionite, or glutamate was the substrate.
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PMID:Action of bacterial lipopolysaccharide on the respiration of mouse liver mitochondria. 698 63

Active immunization of guinea pigs and rabbits with outer membrane proteins (OMP) isolated from Shigella flexneri 3a and Shigella sonnei phase I protected the animals against keratoconjunctivitis shigellosa induced with the homologous or heterologous strain. Protection was also achieved in rabbits after passive immunization with anti-OMP immune serum. Active immunization with lipopolysaccharide of S. flexneri 3a did not protect rabbits against keratoconjunctivitis shigellosa.
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PMID:Protection against keratoconjunctivitis shigellosa induced by immunization with outer membrane proteins of Shigella spp. 700 94

The cell envelope of Shigella sonnei phase I, phase II and R-form was fractionated inot outer and cytoplasmic membrane components by means of sucrose density gradient centrifugation. The protein composition of the outer membrane has been analyzed by SDS-polyacrylamide gel electrophoresis. The outer membrane preparations contained 15-17 proteins. The major proteins of the outer membrane were of apparent molecular weights: 27,000, 28,000 and 31,000. Their amount varied depending on the structural defects of lipopolysaccharide.
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PMID:Outer membrane proteins of Shigella sonnei. I. Characterization of phase I, phase II and R-form Shigella sonnei. 700 62


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