ADP-ribosylation in cultured cells treated with Clostridiumdifficile toxin B

Florin, Inger; Thelestam, Mónica

doi:10.1016/s0006-291x(86)80080-8

Cited by 14 publications

(4 citation statements)

References 15 publications

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“…Toxin B also causes polarization of the nucleus in cells, and it has been suggested that this effect is indirectly due to the disruption of the microfilament system (3). It has been reported that in tissue culture cells the mechanism of action of toxin B is very similar to that of diphtheria toxin (73)(74)(75)230). Additional work is needed, however, to confirm these findings and to further compare the similarities of toxin B and diphtheria toxin.…”

Section: Factors Affecting Toxin Productionmentioning

confidence: 92%

Clostridium difficile: its disease and toxins

1988

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Clostridium difficile is the etiologic agent of pseudomembranous colitis, a severe, sometimes fatal disease that occurs in adults undergoing antimicrobial therapy. The disease, ironically, has been most effectively treated with antibiotics, although some of the newer methods of treatment such as the replacement of the bowel flora may prove more beneficial for patients who continue to relapse with pseudomembranous colitis. The organism produces two potent exotoxins designated toxin A and toxin B. Toxin A is an enterotoxin believed to be responsible for the diarrhea and mucosal tissue damage which occur during the disease. Toxin B is an extremely potent cytotoxin, but its role in the disease has not been as well studied. There appears to be a cascade of events which result in the expression of the activity of these toxins, and these events, ranging from the recognition of a trisaccharide receptor by toxin A to the synergistic action of the toxins and their possible dissemination in the body, are discussed in this review. The advantages and disadvantages of the various assays, including tissue culture assay, enzyme immunoassay, and latex agglutination, currently used in the clinical diagnosis of the disease also are discussed.

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Section: Factors Affecting Toxin Productionmentioning

confidence: 92%

Clostridium difficile: its disease and toxins

1988

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“…In the case of at least one clostridial toxin (C. difficile B toxin [6]), there has been a suggestion that lysosomal processing is needed before the protein expresses its biological activity. The presumed sequence of events is that the endosomes with inactive precursor fuse with lysosomes, after which lysosomal proteases activate the toxin.…”

Section: Resultsmentioning

confidence: 99%

Partial characterization of the enzymatic activity associated with the binary toxin (type C2) produced by Clostridium botulinum

1988

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Clostridium botulinum produces a binary toxin that possesses a heavy chain (-100,000 daltons) and a light chain (-50,000 daltons). The heavy chain is a binding component that directs the toxin to vulnerable cells, and the light chain is an enzyme that has mono(ADP-ribosyl)ating activity. A number of experiments have been done to help characterize the enzymatic activity of the toxin. The data reveal that the enzyme has a pH optimum within the range of 7.0 to 8.0. It is not inhibited or stimulated by physiological concentrations of sodium, potassium, calcium, or magnesium. The enzyme is inhibited by high concentrations of salt, however, as well as high concentrations of nicotinamide, thymidine, theophylline, and histamine; and it is stimulated by histone and lysolecithin. Boiling irreversibly denatures the light chain of the toxin, but denaturation caused by guanidine and urea is substantially reversible. Enzymatic activity is not altered by short exposure to lysosomal proteases, including cathepsin B, cathepsin H, dipeptidyl aminopeptidase, and catheptic carboxypeptidase B.

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“…Cytopathogenic effects are thwarted by inhibitors of the energy metabolism after the endocytosis is completed [53]. ADPribosylation was reported as a property of the toxin [23]. This would mean that the toxin has similar properties as the cholera toxin A subunit and E. coli heat-labile enterotoxin [38].…”

Section: Toxin Bmentioning

confidence: 99%

“…Still, it remains difficult to assign specific functions to these toxins. History has shown that in several cases incorrect assignments were made: glutamate dehydrogenasc was used in a test to detect toxin A [21], cnolasc was reported as a property of toxin B [22] and ADPribosylation was later shown not to be a characteristic of toxin B [23,24].SSDI 0168-6445(93)E0067-T…”

mentioning

confidence: 99%

Toxins A and B of Clostridium difficile

Wolfhagen¹

1994

FEMS Microbiology Reviews

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Abstract:The toxins produced by Clostridium dtfficile share several functional properties with other bacterial toxins, like the heat-labile enterotoxin of Escherichia coli and cholera toxin. However, functional and structural differences also exist. Like cholera toxin, their main target is the disruption of the microfilaments in the cell. However, since these effects are not reversible, as found with cholera toxin, additional mechanisms add to the cytotoxic potential of these toxins. Unlike most bacterial toxins, which are built from two structurally and functionally different small polypeptide chains, the functional and binding properties of the toxins of C. di['licile are confined within one large polypeptide chain, making them the largest bacterial toxins known so far.

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ADP-ribosylation in cultured cells treated with Clostridiumdifficile toxin B

Cited by 14 publications

References 15 publications

Clostridium difficile: its disease and toxins

Clostridium difficile: its disease and toxins

Partial characterization of the enzymatic activity associated with the binary toxin (type C2) produced by Clostridium botulinum

Toxins A and B of Clostridium difficile

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