Characterization of the carbohydrate receptors of the Clostridium difficile enterotoxin

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dc.contributor.authorTucker, Kenneth D.en
dc.contributor.committeechairWilkins, Tracy D.en
dc.contributor.committeememberGregory, Eugene "Mick"en
dc.contributor.committeememberJohnson, J.L.en
dc.contributor.committeememberKrieg, Noel R.en
dc.contributor.committeememberSmibert, R.M.en
dc.contributor.departmentMicrobiologyen
dc.date.accessioned2014-03-14T21:10:51Zen
dc.date.adate2006-05-11en
dc.date.available2014-03-14T21:10:51Zen
dc.date.issued1990en
dc.date.rdate2006-05-11en
dc.date.sdate2006-05-11en
dc.description.abstractClostridium difficile causes pseudomembranous colitis in humans and a similar ileocecitis in hamsters. This organism can colonize the intestines after antibiotic therapy disrupts the normal intestinal microflora. Once established in the intestines, the organism causes disease by producing two toxins, designated toxin A and toxin B. Only toxin A is active on intestinal epithelium, thus toxin A is the cause of the initial tissue damage in the intestines. In order for a toxin to affect a cell, it must first bind to the cell. Toxin A has been shown to bind to Galα1- 3Galβ 1-4GIcNAc on the intestinal epithelium of hamsters. I provide evidence that toxin A can use this trisaccharide as a functional receptor on cell lines, and that the expression of the carbohydrate receptor increases the sensitivity of the cells to toxin A. Furthermore, the intestinal epithelium of infant hamsters bound less toxin A at 37C than did the adult tissue, and infants are less sensitive to the disease caused by C. difficile than are adults. This provides further evidence that the activity of toxin A is increased by the binding of the toxin to Galα1-3Galβ1- 4GlcNAc. Even though Galα1-3Galβ 1-4GlcNAc was a receptor for toxin A on animal cells, it probably is not a receptor for toxin A in humans, because people do not normally express this carbohydrate. Instead, I found that toxin A bound to the carbohydrate antigens designated I, X, and Y, which are present on the intestinal epithelium of humans. These carbohydrates could be receptors for toxin A. The possible significance of these receptors is discussed.en
dc.description.degreePh. D.en
dc.format.extentviii, 144 leavesen
dc.format.mediumBTDen
dc.format.mimetypeapplication/pdfen
dc.identifier.otheretd-05112006-154746en
dc.identifier.sourceurlhttp://scholar.lib.vt.edu/theses/available/etd-05112006-154746/en
dc.identifier.urihttp://hdl.handle.net/10919/37739en
dc.language.isoenen
dc.publisherVirginia Techen
dc.relation.haspartLD5655.V856_1990.T834.pdfen
dc.relation.isformatofOCLC# 22354907en
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subject.lccLD5655.V856 1990.T834en
dc.subject.lcshAntibiotics -- Side effectsen
dc.subject.lcshDiarrhea -- Treatmenten
dc.titleCharacterization of the carbohydrate receptors of the <i>Clostridium difficile</i> enterotoxinen
dc.typeDissertationen
dc.type.dcmitypeTexten
thesis.degree.disciplineMicrobiologyen
thesis.degree.grantorVirginia Polytechnic Institute and State Universityen
thesis.degree.leveldoctoralen
thesis.degree.namePh. D.en

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