Role of
            <i>Vibrio cholerae</i>
            O139 Surface Polysaccharides in Intestinal Colonization

Nesper, Jutta; Schild, Stefan; Lauriano, Crystal M.; Kraiss, Anita; Klose, Karl E.; Reidl, Joachim

doi:10.1128/iai.70.11.5990-5996.2002

Cited by 55 publications

(65 citation statements)

References 47 publications

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“…The BasR-regulated genes for lipid A modification are upregulated by bile salts. While efflux is a vital means of resisting the deleterious effects of bile, limiting penetration by altering the composition of the outer membrane is an additional strategy used by many bacteria (42,49,57). The genes encoding the BasR-BasS (also known as PmrA-PmrB) histidine kinase TCRS were upregulated by BSM treatment on our microarray and by our confirmatory methods (Table 1 and Fig.…”

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confidence: 78%

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Bile Salts Induce Resistance to Polymyxin in Enterohemorrhagic Escherichia coliO157:H7

et al. 2011

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Many enteric bacteria use bile as an environmental cue to signal resistance and virulence gene expression. Microarray analysis of enterohemorrhagic Escherichia coli O157:H7 (EHEC) treated with bile salts revealed upregulation of genes for an efflux system (acrAB), a two-component signal transduction system (basRS/ pmrAB), and lipid A modification (arnBCADTEF and ugd). Bile salt treatment of EHEC produced a basS-and arnT-dependent resistance to polymyxin.

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confidence: 78%

“…The RND efflux systems have been well described as playing a significant role in bile resistance among Gram-negative bacteria (45). Additionally, the use of two-component regulatory systems (TCRS) (52,68) and alterations of the lipopolysaccharide (LPS) layer have been shown to be involved in resistance to bile in several bacteria (8,42,43,49,71).…”

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confidence: 99%

Bile Salts Induce Resistance to Polymyxin in Enterohemorrhagic Escherichia coliO157:H7

et al. 2011

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“…O-antigen-negative strains were found to be sensitive to complement and cationic peptides, but they displayed significant resistance to bile salts and short-chain organic acids. In another study, loss of LPS O side chain or capsular polysaccharide in V. cholerae O139 strains resulted in a significant reduction in colonization of the infant mouse small intestine, indicating that the presence of both LPS O side chain and capsular polysaccharide is important during the colonization process (19).…”

Section: Discussionmentioning

confidence: 99%

Effect of Phage on the Infectivity of Vibrio cholerae and Emergence of Genetic Variants

et al. 2008

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Seasonal epidemics of cholera in Bangladesh are self-limited in nature, presumably due to phage predation of the causative Vibrio cholerae during the late stage of an epidemic, when cholera patients excrete large quantities of phage in their stools. To further understand the mechanisms involved, we studied the effect of phage on the infectivity and survival of V. cholerae shed in stools. The 50% infectious dose of stool vibrios in infant mice was ϳ10-fold higher when the stools contained a phage (1.8 ؋ 10 3 to 5.7 ؋ 10 6 PFU/ml) than when stools did not contain a detectable phage. In competition assays in mice using a reference strain and phage-negative cholera stools, the infectivity of biofilm-like clumped cells was 3.9-to 115.9-fold higher than that of the corresponding planktonic cells. However, the difference in infectivity of these two cell populations in phage-positive stools was significantly less than that in phage-negative stools (P ‫؍‬ 0.0006). Coculture of a phage and V. cholerae or dilutions of phage-positive cholera stools in nutrient medium, but not in environmental water, caused rapid emergence of phage-resistant derivatives of the bacteria, and these derivatives lost their O1 antigen. In cholera stools and in intestinal contents of mice prechallenged with a mixture of V. cholerae and phage, the bacteria remained completely phage susceptible, suggesting that the intestinal environment did not favor the emergence of phage-resistant derivatives that lost the O1 antigen. Our results indicate that phages lead to the collapse of epidemics by modulating the required infectious dose of the bacteria. Furthermore, the dominance of phage-resistant variants due to the bactericidal selective mechanism occurs rarely in natural settings, and the emerging variants are thus unable to sustain the ongoing epidemic.

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“…LPS is involved in cell adhesion, organ colonization, and resistance against antimicrobial effector molecules in many different pathogens, including Brucella melitensis 16M (10), Salmonella enterica serovar Typhi (26), Vibrio cholerae O139 (29), and serovar Typhimurium (6,22). Although many studies investigated the role of LPS in systemic serovar Typhimurium virulence (22,30), little is known about the requirement of O-antigen side chains in enteric infection, e.g., induction of colitis.…”

Section: Discussionmentioning

confidence: 99%

O-Antigen-NegativeSalmonella entericaSerovar Typhimurium Is Attenuated in Intestinal Colonization but Elicits Colitis in Streptomycin-Treated Mice

et al. 2009

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Lipopolysaccharide (LPS) is a major constituent of the outer membrane and an important virulence factor of Salmonella enterica subspecies 1 serovar Typhimurium (serovar Typhimurium). To evaluate the role of LPS in eliciting intestinal inflammation in streptomycin-treated mice, we constructed an O-antigen-deficient serovar Typhimurium strain through deletion of the wbaP gene. The resulting strain was highly susceptible to human complement activity and the antimicrobial peptide mimic polymyxin B. Furthermore, it showed a severe defect in motility and an attenuated phenotype in a competitive mouse infection experiment, where the ⌬wbaP strain (SKI12) was directly compared to wild-type Salmonella. Nevertheless, the ⌬wbaP strain (SKI12) efficiently invaded HeLa cells in vitro and elicited acute intestinal inflammation in streptomycin-pretreated mice. Our experiments prove that the presence of complete LPS is not essential for in vitro invasion or for triggering acute colitis.

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Role of Vibrio cholerae O139 Surface Polysaccharides in Intestinal Colonization

Cited by 55 publications

References 47 publications

Bile Salts Induce Resistance to Polymyxin in Enterohemorrhagic Escherichia coliO157:H7

Bile Salts Induce Resistance to Polymyxin in Enterohemorrhagic Escherichia coliO157:H7

Effect of Phage on the Infectivity of Vibrio cholerae and Emergence of Genetic Variants

O-Antigen-NegativeSalmonella entericaSerovar Typhimurium Is Attenuated in Intestinal Colonization but Elicits Colitis in Streptomycin-Treated Mice

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