Role of Somatic Antigen of Vibrio Cholerae in Adhesion to Intestinal Mucosa

Chitnis, DS; Sharma, Kamal Dev; Kamat, R. S.

doi:10.1099/00222615-15-1-53

Cited by 38 publications

(20 citation statements)

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“…Motility does not appear to be essential during human infection according to the ability of a nonmotile vaccine strain (Peru-15) to colonize volunteers, but may be required for optimal levels of infectivity [19,20]. V. cholerae utilizes adhesion factors, some of which may remain to be elucidated, but may include: O1 LPS [21]; GlcNAc-binding protein (GbpA) [22]; a protein (TcpF) secreted by the toxin coregulated pilus (TCP) biogenesis apparatus [23]; outer membrane protein OmpU [24]; and cholera toxin (CT), although this has only been implicated in an adult rabbit model [25]. TCP facilitates interbacterial interactions that are important for colonization [26,27].…”

Section: Cholera Pathogenesis and Transmissionmentioning

confidence: 99%

Vibrio cholerae: lessons for mucosal vaccine design

Bishop

Camilli

2011

Expert Review of Vaccines

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The ability of Vibrio cholerae to persist in bodies of water will continue to confound our ability to eradicate cholera through improvements to infrastructure, and thus cholera vaccines are needed. We aim for an inexpensive vaccine that can provide long-lasting protection from all epidemic cholera infections, currently caused by O1 or O139 serogroups. Recent insights into correlates of protection, epidemiology and pathogenesis may help us design improved vaccines. This notwithstanding, we have come to appreciate that even marginally protective vaccines, such as oral whole-cell killed vaccines, if widely distributed, can provide significant protection, owing to herd immunity. Further efforts are still required to provide more effective protection of young children. Keywords cholera; classical; El Tor; IgA; protection; vaccine; Vibrio cholerae; vibriocidal Cholera prevention by vaccinationCholera is mainly a fecal-orally transmitted disease and humans are the only known natural veterbrate host. Cholera has been endemic in southern Asia since recorded history. Cholera has spread globally in seven pandemic waves since 1817, of which the current one began in 1961. In 2008, the WHO reported 190,130 cholera cases worldwide, associated with 5143 deaths (98% in Africa), but cholera is globally under-reported and the true disease burden is estimated to be in the millions [1,2]. In countries such as Bangladesh, cholera is endemic and both the rural and urban population is afflicated with biannual outbreaks [3]. In addition to endemic outbreaks, sporadic outbreaks can occur whenever sanitation and clean water provisions are lacking, such as occurred in Zimbabwe in [2008][2009] following the collapse of infrastructure [2].A lack of good animal models for immunization and challenge has hampered the study of cholera vaccines. For example, adult mice are refractory to acute cholera, but infant mice up to 1 week of age are permissive for intestinal colonization [4]. Therefore, passive protection models have been developed, either using immunization of adult female mice and challenge of their pups, which are protected by sucking, or mixing antibodies with Vibrio cholerae in © 2011 Expert Reviews Ltd † Author for correspondence: Tel.: +1 617 636 2144, Fax: +1 617 636 2175, andrew.camilli@tufts.edu. Financial & competing interests disclosureThe authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. No writing assistance was utilized in the production of this manuscript. NIH Public Access Author ManuscriptExpert Rev Vaccines. Author manuscript; available in PMC 2011 November 1. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript vitro prior to infection [5,6]. Despite the limitations of preclinical models, a number of cholera vaccines have been developed (discussed in detail later).Since 1999, the WHO has advocated the use of oral cholera vac...

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Section: Cholera Pathogenesis and Transmissionmentioning

confidence: 99%

Vibrio cholerae: lessons for mucosal vaccine design

Bishop

Camilli

2011

Expert Review of Vaccines

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“…The flagellum thus functions as a carrier for moieties promoting adherence. That LPS may be one of these moieties is suggested by the finding that LPS can inhibit adhesion of V. cholerae to intestinal mucosa (5), that anti-LPS antibodies can protect against experimental cholera (22), and that immunity against mucosal colonization in a rat model has been found to be accompanied at least in some cases by mucus-borne antibody against LPS (6). Non-LPS adhesins may also occur on the flagellum, however, including those which might be exposed where sheath is removed.…”

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“…Labeling was associated with the sheath of the flagellum rather than the core, and flagellar cores were not labeled. Flagellum and cell shared a common set of lipopolysaccharide antigens characteristic of the strain serotype.Recent research on the pathogenesis of cholera has concentrated on the factors responsible for adhesion of Vibrio cholerae cells to the intestinal mucosa and the nature of the antigens responsible for stimulating an immune response to infection (1,(4)(5)(6)20). Although the important protective antigens have yet to be unequivocally defined, purified lipopolysaccharide (LPS) has been reported to induce significant protection against cholera in humans and experimental animals (16).…”

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Demonstration of lipopolysaccharide on sheathed flagella of Vibrio cholerae O:1 by protein A-gold immunoelectron microscopy

Fuerst

Perry

1988

J Bacteriol

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Monoclonal antibodies with group and type specificity for lipopolysaccharide antigens were used in combination with protein A-colloidal gold labeling and transmission electron microscopy to demonstrate the presence of lipopolysaccharide antigens on both the sheathed flagellum and the cel surface of Inaba and Ogawa strains of Vibrio cholerae 0:1. Labeling was associated with the sheath of the flagellum rather than the core, and flagellar cores were not labeled. Flagellum and cell shared a common set of lipopolysaccharide antigens characteristic of the strain serotype.Recent research on the pathogenesis of cholera has concentrated on the factors responsible for adhesion of Vibrio cholerae cells to the intestinal mucosa and the nature of the antigens responsible for stimulating an immune response to infection (1,(4)(5)(6)20). Although the important protective antigens have yet to be unequivocally defined, purified lipopolysaccharide (LPS) has been reported to induce significant protection against cholera in humans and experimental animals (16). The flagellum of V. cholerae has been implicated in pathogenesis of cholera in two ways: with respect to its role as a motility organelle (12,18,25) and with respect to its possible role in adherence of V. cholerae to the host intestinal surface (1). The role of the flagellum as a carrier of the adhesins responsible for attachment to intestinal tissue may be of greater significance than its role in conferring motility (1).While the flagellum of V. cholerae is of possible significance in pathogenesis, its chemical and antigenic composition are poorly understood. The flagellum possesses a membranous sheath covering a core which is similar in structure to naked flagella of other bacteria (7,8). In Vibrio metchnikovii, continuity between the sheath and the outer membrane has been demonstrated (10). The question of whether the flagellar sheath of V. cholerae shares the macromolecular composition of the cell wall outer membrane has not been resolved, however. It has been proposed, on the basis of immunoferritin electron microscopy using polyclonal antibodies to LPS, that the sheath does not contain LPS and that the sheath is thus not a simple extension of the outer membrane (17). However, reports that polyclonal antibodies against somatic 0 antigen and monoclonal antibodies against LPS determinants immobilize motile V. cholerae cells are consistent with the occurrence of LPS in the flagellar sheath (1,14). One way to resolve this problem is to localize LPS directly, utilizing highly specific monoclonal antibodies against LPS antigenic determinants and an electron-dense protein A-gold marker for immunoelectron microscopy. LPS determinants distinguish two major serotypes of V. cholerae 0:1: Ogawa, with determinants A and B, and Inaba, with determinants A and C (13). The establishment of hybrid cell lines producing monoclonal antibodies against such groupand type-specific 0 antigens of V. cholerae 0:1 (13,15) Serotypes were checked routinely by slide agglutination with polytypic (an...

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“…In order to cause the disease, V. cholerae must adhere to the intestinal mucus barrier (52). The ability of V. cholerae to adhere to animal cells has been studied before (26,42), and various adherence factors have been proposed, including the virulence-associated toxin-coregulated pilus (5), outer membrane proteins (26,42), and lipopolysaccharide (LPS) (11). Attachment of V. cholerae to abiotic surfaces has also been recently described (50).…”

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Intestinal Adherence of Vibrio cholerae Involves a Coordinated Interaction between Colonization Factor GbpA and Mucin

et al. 2008

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The chitin-binding protein GbpA of Vibrio cholerae has been recently described as a common adherence factor for chitin and intestinal surface. Using an isogenic in-frame gbpA deletion mutant, we first show that V. cholerae O1 El Tor interacts with mouse intestinal mucus quickly, using GbpA in a specific manner. The gbpA mutant strain showed a significant decrease in intestinal adherence, leading to less colonization and fluid accumulation in a mouse in vivo model. Purified recombinant GbpA (rGbpA) specifically bound to N-acetyl-D-glucosamine residues of intestinal mucin in a dose-dependent, saturable manner with a dissociation constant of 11.2 M. Histopathology results from infected mouse intestine indicated that GbpA binding resulted in a time-dependent increase in mucus secretion. We found that rGbpA increased the production of intestinal secretory mucins (MUC2, MUC3, and MUC5AC) in HT-29 cells through upregulation of corresponding genes. The upregulation of MUC2 and MUC5AC genes was dependent on NF-B nuclear translocation. Interestingly, mucin could also increase GbpA expression in V. cholerae in a dose-dependent manner. Thus, we propose that there is a coordinated interaction between GbpA and mucin to upregulate each other in a cooperative manner, leading to increased levels of expression of both of these interactive factors and ultimately allowing successful intestinal colonization and pathogenesis by V. cholerae.Vibrio cholerae is the causative agent of the potentially lethal disease cholera. V. cholerae strains belonging to serogroups O1 and O139 are mainly responsible for cholera epidemics, while strains of other serogroups may cause sporadic outbreaks of the disease. Although the O139 strain has evolved recently, V. cholerae O1 biotype El Tor strains have still been responsible for most of the epidemics in recent years (20,26). In order to cause the disease, V. cholerae must adhere to the intestinal mucus barrier (52). The ability of V. cholerae to adhere to animal cells has been studied before (26,42), and various adherence factors have been proposed, including the virulence-associated toxin-coregulated pilus (5), outer membrane proteins (26, 42), and lipopolysaccharide (LPS) (11). Attachment of V. cholerae to abiotic surfaces has also been recently described (50). However, there is still no information about the factor(s) responsible for initial adherence of the bacteria to the intestine and whether the host plays any role in aiding the colonization of the intestine by the bacteria.Vibrios are marine organisms that adhere to chitin in the environment (12, 33) and utilize chitin as the sole source of nitrogen and carbon by using a family of glycosyl hydrolases, called chitinases (21). Genome analysis of V. cholerae O1 El Tor has revealed the presence of seven such chitinase genes (7), some of which have been characterized (27,37). One of these genes is the putative chitinase gene with locus number VCA0811, the product of which has been recently identified as a common adhesion molecule for both chitinou...

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Role of Somatic Antigen of Vibrio Cholerae in Adhesion to Intestinal Mucosa

Cited by 38 publications

References 6 publications

Vibrio cholerae: lessons for mucosal vaccine design

Vibrio cholerae: lessons for mucosal vaccine design

Demonstration of lipopolysaccharide on sheathed flagella of Vibrio cholerae O:1 by protein A-gold immunoelectron microscopy

Intestinal Adherence of Vibrio cholerae Involves a Coordinated Interaction between Colonization Factor GbpA and Mucin

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