Studies on adhesion, haemagglutination and other biological properties of Vibrio cholerae O139

Sasmal, D.

doi:10.1016/0928-8244(94)00084-7

Cited by 3 publications

(3 citation statements)

References 8 publications

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“…Furthermore, subcutaneous injection of CT in guinea pigs and rabbits leads to vascular effusion (Craig, 1965), which has been used as a criterion for assessing virulence of V.c. isolates (Sasmal et al, 1995). …”

Section: Discussionmentioning

confidence: 99%

Cholera Toxin Disrupts Barrier Function by Inhibiting Exocyst-Mediated Trafficking of Host Proteins to Intestinal Cell Junctions

Guichard

Cruz-Moreno

Aguilar

et al. 2013

Cell Host & Microbe

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Summary Cholera toxin (CT), a virulence factor elaborated by Vibrio cholerae, is sufficient to induce the severe diarrhea characteristic of cholera. The enzymatic moiety of CT (CtxA) increases cAMP synthesis in intestinal epithelial cells, leading to chloride ion (Cl−) efflux through the CFTR Cl− channel. To preserve electroneutrality and osmotic balance, sodium ions and water also flow into the intestinal lumen via a paracellular route. We find that CtxA-driven cAMP increase also inhibits Rab11/exocyst-mediated trafficking of host proteins including E-cadherin and Notch signaling components to cell-cell junctions in Drosophila, human intestinal epithelial cells, and ligated mouse ileal loops, thereby disrupting barrier function. Additionally, CtxA induces junctional damage, weight loss, and dye leakage in the Drosophila gut, contributing to lethality from live V. cholerae infection, all of which can be rescued by Rab11 over-expression. These barrier-disrupting effects of CtxA may act in parallel with Cl− secretion to drive the pathophysiology of cholera.

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Section: Discussionmentioning

confidence: 99%

Cholera Toxin Disrupts Barrier Function by Inhibiting Exocyst-Mediated Trafficking of Host Proteins to Intestinal Cell Junctions

Guichard

Cruz-Moreno

Aguilar

et al. 2013

Cell Host & Microbe

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“…ml 21 in PBS. Biotinylation was carried out as described previously (Sasmal et al, 1995). After three washes with PBS, biotinylated bacterial suspension (100 ml per well) at a fixed concentration (~5610 6 c.f.u.…”

Section: Methodsmentioning

confidence: 99%

Allelic variation in colonization factor CS6 of enterotoxigenic Escherichia coli isolated from patients with acute diarrhoea and controls

Sabui

Ghosal

Dutta

et al. 2010

Journal of Medical Microbiology

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Colonization factor antigens (CFAs) are important virulence factors in enterotoxigenic Escherichia coli (ETEC). Using a multiplex PCR and RT-PCR, this study tested the presence of common colonization factor-encoding genes and their expression in 50 ETEC strains isolated from stool specimens. The samples were from patients (children) with acute diarrhoea (cases) admitted to the Infectious Disease Hospital (Kolkata, India) and from normal children (controls) under 5 years of age from the community. The results indicated that coli surface antigen 6 (CS6) was the most prevalent CFA (78 %) expressed by these ETEC strains. Sequence analysis of both of the CS6 structural genes, i.e. cssA and cssB, in different ETEC isolates revealed the presence of point mutations in a systematic fashion. Based on the analysis of these variations, it was found that CssA had three alleles and CssB had two. Based on the allelic variations, subtyping of CS6 into AIBI, AIIBII, AIIIBI, AIBII and AIIIBII is proposed. The point mutations in the different alleles were reflected in a partial alteration in the secondary structure of both subunits, as determined by computational analysis. The functional significance of these changes was confirmed with cellular binding studies in Caco-2 cells with representative ETEC isolates. CS6 with AI or AIII allelic subtypes showed a higher binding capacity than AII, whereas BI showed stronger binding than BII. The AII and BII alleles were mostly detected in controls rather than in cases. The antibody specificity of BI and BII also varied due to alteration of the amino acids. Thus, CS6 variants are formed as a result of different allelic combinations of CssA and CssB, and these changes at the functional level might be important in the development of an effective ETEC vaccine.

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“…The result is an increased allergic response with lower dosage of the allergen needed. For this reason CT is often used as a mucosal adjuvant (Kaper et al, 1995;Keusch et al, 1967;Lange et al, 1998;Sack et al, 2004;Sasmal et al, 1995;Yardley and Brown, 1973). Furthermore, CT has been shown to stimulate strong responses to mucosally delivered antigens, by inducing an antigen-specific type 2 response (Bashir et al, 2002;Christensen et al, 2003;Helm et al, 2002;Li et al, 2000;Li et al, 2001;Williams et al, 1999) or a mixed Th1 + Th2 response (Hornquist and Lycke, 1993;Marinaro et al, 1995), with a bias toward Th2 (Marinaro et al, 1995;Wilson et al, 1991;Xu-Amano et al, 1993).…”

Section: Cholera Toxinmentioning

confidence: 99%

Advancement of the Brown Norway rat as a model for food allergy : route of exposure - immunomodulation - allergogenomics

Jonge¹

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Studies on adhesion, haemagglutination and other biological properties of Vibrio cholerae O139

Cited by 3 publications

References 8 publications

Cholera Toxin Disrupts Barrier Function by Inhibiting Exocyst-Mediated Trafficking of Host Proteins to Intestinal Cell Junctions

Cholera Toxin Disrupts Barrier Function by Inhibiting Exocyst-Mediated Trafficking of Host Proteins to Intestinal Cell Junctions

Allelic variation in colonization factor CS6 of enterotoxigenic Escherichia coli isolated from patients with acute diarrhoea and controls

Advancement of the Brown Norway rat as a model for food allergy : route of exposure - immunomodulation - allergogenomics

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