Occurrence of 2-O-Methyl-N-(3-Deoxy-L-glycero-tetronyl)-D-perosamine (4-amino-4,6-dideoxy-D-manno-pyranose) in Lipopolysaccharide from Ogawa but Not from Inaba O Forms of O1 Vibrio cholerae

Hisatsune, Kazuhito; Kondo, Seiichi; Isshiki, Yasunori; Iguchi, Takehiro; Haishima, Y.

doi:10.1006/bbrc.1993.1046

Cited by 101 publications

(61 citation statements)

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“…O1 LPS is composed of 15 to 18 repeating units of the disaccharide perosamine (20,73). As mentioned above, O1 Ogawa O antigen differs from O1 Inaba only by the presence of a methyl group (37). In contrast, O139 terminal O antigen is composed of a single hexasaccharide unit resulting in a short LPS (38).…”

Section: Resultsmentioning

confidence: 99%

“…Currently, cholera outbreaks are caused by the El Tor biotype of O1, which in Bangladesh by 1989 had replaced the previously circulating classical biotype (49). The O1 serogroup includes two subtypes, serotypes Ogawa and Inaba, which differ only by the presence of a 2-O-methyl group in the Ogawa O antigen (37). O139 appeared in 1993 and to date is the only non-O1 serogroup to have caused a major cholera epidemic (23,64).…”

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confidence: 99%

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Mucosal Immunization with Vibrio cholerae Outer Membrane Vesicles Provides Maternal Protection Mediated by Antilipopolysaccharide Antibodies That Inhibit Bacterial Motility

et al. 2010

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Vibrio cholerae is the causative agent of cholera, a severe diarrheal disease that remains endemic in many parts of the world and can cause outbreaks wherever sanitation and clean water systems break down. Prevention of disease could be achieved through improved sanitation and clean water provision supported by vaccination. V. cholerae serogroup O1 is the major cause of cholera; O1 serotypes Inaba and Ogawa have similar disease burdens, while O139 is the only non-O1 serogroup to cause epidemics. We showed previously that immunization of adult female mice with purified V. cholerae outer membrane vesicles (OMVs) elicits an antibody response that protect neonates from oral V. cholerae challenge and that suckling from an immunized dam accounts for the majority of protection from V. cholerae colonization. Here we report that lipopolysaccharide (LPS) is the major OMV protective antigen. Mucosal immunization with OMVs from Inaba or Ogawa provides significant cross-serotype protection from V. cholerae colonization, although serotype-specific antigens are dominant. OMVs from O1 or O139 do not provide cross-serogroup protection, but by immunization with a mixture of O1 and O139 OMVs, cross-serogroup protection was achieved. Neonatal protection is not associated with significant bacterial death but may involve inhibition of motility, as antibodies from OMVimmunized mice inhibit V. cholerae motility in vitro, with trends that parallel in vivo protection. Motility assays also reveal that a higher antibody titer is required to immobilize O139 compared to O1, a phenotype that is O139 capsule dependent.

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

Mucosal Immunization with Vibrio cholerae Outer Membrane Vesicles Provides Maternal Protection Mediated by Antilipopolysaccharide Antibodies That Inhibit Bacterial Motility

et al. 2010

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“…The O-SP terminal sugar of V. cholerae LPS is now known to differentiate Ogawa and Inaba serotypes. V. cholerae O-SP consists of (132)-␣-linked 4-amino-4,6-dideoxy-D-mannose (perosamine) whose amino group is acylated with 3-deoxy-L-glycero-tetronic acid (17,21). In the Ogawa O-SP, the terminal sugar is characterized by a 2-O-methyl group, while the terminal sugar in the Inaba O-SP has a hydroxyl at the 2 position (17,18,40,41).…”

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confidence: 99%

Synthetic Fragments ofVibrio choleraeO1 Inaba O-Specific Polysaccharide Bound to a Protein Carrier Are Immunogenic in Mice but Do Not Induce Protective Antibodies

Meeks¹,

Saksena

et al. 2004

Infect Immun

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Development of Vibrio cholerae lipopolysaccharide (LPS) as a cholera vaccine immunogen is justified by the correlation of vibriocidal anti-LPS response with immunity. Two V. cholerae O1 LPS serotypes, Inaba and Ogawa, are associated with endemic and pandemic cholera. Both serotypes induce protective antibody following infection or vaccination. Structurally, the LPSs that define the serotypes are identical except for the terminal perosamine moiety, which has a methoxyl group at position 2 in Ogawa but a hydroxyl group in Inaba. The terminal sugar of the Ogawa LPS is a protective B-cell epitope. We chemically synthesized the terminal hexasaccharides of V. cholerae serotype Ogawa, which comprises in part the O-specific polysaccharide component of the native LPS, and coupled the oligosaccharide at different molar ratios to bovine serum albumin (BSA). Our initial studies with Ogawa immunogens showed that the conjugates induced protective antibody. We hypothesized that antibodies specific for the terminal sugar of Inaba LPS would also be protective. Neoglycoconjugates were prepared from synthetic Inaba oligosaccharides (disaccharide, tetrasaccharide, and hexasaccharide) and BSA at different levels of substitution. BALB/c mice responded to the Inaba carbohydrate (CHO)-BSA conjugates with levels of serum antibodies of comparable magnitude to those of mice immunized with Ogawa CHO-BSA conjugates, but the Inaba-specific antibodies (immunoglobulin M [IgM] and IgG1) were neither vibriocidal nor protective in the infant mouse cholera model. We hypothesize that the anti-Inaba antibodies induced by the Inaba CHO-BSA conjugates have enough affinity to be screened via enzyme-linked immunosorbent assay but not enough to be protective in vivo.

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“…The LPS also contains the carbohydrate quinovosamine, which at the present time cannot be precisely defined as a component of either the O antigen or the core oligosaccharide (45). The Ogawa and Inaba serotypes differ by the presence of a 2-Omethyl group in the nonreducing terminal carbohydrate in the Ogawa O antigen (19,21). It was shown that Ogawa and Inaba O1 LPS can interconvert and that this serotype variation is due to spontaneous mutations in the wbeT gene (47).…”

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confidence: 99%

Characterization ofVibrio choleraeO1 Antigen as the Bacteriophage K139 Receptor and Identification of IS1004Insertions Aborting O1 Antigen Biosynthesis

Nesper¹,

Kapfhammer²,

Klose

et al. 2000

J Bacteriol

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Bacteriophage K139 was recently characterized as a temperate phage of O1 Vibrio cholerae. In this study we have determined the phage adsorption site on the bacterial cell surface. Phage-binding studies with purified lipopolysaccharide (LPS) of different O1 serotypes and biotypes revealed that the O1 antigen serves as the phage receptor. In addition, phage-resistant O1 El Tor strains were screened by using a virulent isolate of phage K139. Analysis of the LPS of such spontaneous phage-resistant mutants revealed that most of them synthesize incomplete LPS molecules, composed of either defective O1 antigen or core oligosaccharide. By applying phage-binding studies, it was possible to distinguish between receptor mutants and mutations which probably caused abortion of later steps of phage infection. Furthermore, we investigated the genetic nature of O1-negative strains by Southern hybridization with probes specific for the O antigen biosynthesis cluster (rfb region). Two of the investigated O1 antigen-negative mutants revealed insertions of element IS1004 into the rfb gene cluster. Treating one wbeW::IS1004 serum-sensitive mutant with normal human serum, we found that several survivors showed precise excision of IS1004, restoring O antigen biosynthesis and serum resistance. Investigation of clinical isolates by screening for phage resistance and performing LPS analysis of nonlysogenic strains led to the identification of a strain with decreased O1 antigen presentation. This strain had a significant reduction in its ability to colonize the mouse small intestine.Vibrio cholerae strains from serogroups O1 and O139 are the etiologic agents of cholera, a life-threatening acute diarrhea. The O1 serogroup is divided into the main serotypes Inaba and Ogawa, and O1 is subdivided into two distinct biotypes, designated classical and El Tor (22). Lipopolysaccharide (LPS) is the major integral component of the outer membrane and chemically consists of an O antigen, a core oligosaccharide, and lipid A. The O antigen of O1 V. cholerae consists of a homopolymer of approximately 18 (132) linked linear 4-(3-deoxy-L-glycero-tetronamido)-4,6-dideoxy-D-mannose) (23, 36). The LPS also contains the carbohydrate quinovosamine, which at the present time cannot be precisely defined as a component of either the O antigen or the core oligosaccharide (45). The Ogawa and Inaba serotypes differ by the presence of a 2-Omethyl group in the nonreducing terminal carbohydrate in the Ogawa O antigen (19,21). It was shown that Ogawa and Inaba O1 LPS can interconvert and that this serotype variation is due to spontaneous mutations in the wbeT gene (47). Strains of the serogroup O139 contain only a short O antigen but, in contrast to O1 strains, are encapsulated (51). Molecular and epidemiological analyses as well as phage typing revealed that O139 strains are very similar to O1 El Tor strains (2,17,18). One characteristic difference is the replacement of the 22-kb O1 rfb region with a 35-kb DNA fragment encoding the O139 O antigen and capsule (4,5,10,48)...

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Occurrence of 2-O-Methyl-N-(3-Deoxy-L-glycero-tetronyl)-D-perosamine (4-amino-4,6-dideoxy-D-manno-pyranose) in Lipopolysaccharide from Ogawa but Not from Inaba O Forms of O1 Vibrio cholerae

Cited by 101 publications

References 0 publications

Mucosal Immunization with Vibrio cholerae Outer Membrane Vesicles Provides Maternal Protection Mediated by Antilipopolysaccharide Antibodies That Inhibit Bacterial Motility

Mucosal Immunization with Vibrio cholerae Outer Membrane Vesicles Provides Maternal Protection Mediated by Antilipopolysaccharide Antibodies That Inhibit Bacterial Motility

Synthetic Fragments ofVibrio choleraeO1 Inaba O-Specific Polysaccharide Bound to a Protein Carrier Are Immunogenic in Mice but Do Not Induce Protective Antibodies

Characterization ofVibrio choleraeO1 Antigen as the Bacteriophage K139 Receptor and Identification of IS1004Insertions Aborting O1 Antigen Biosynthesis

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