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dc.contributor.advisorTukel, Cagla
dc.creatorBiesecker, Steven
dc.date.accessioned2020-10-20T13:33:35Z
dc.date.available2020-10-20T13:33:35Z
dc.date.issued2012
dc.identifier.other864885404
dc.identifier.urihttp://hdl.handle.net/20.500.12613/798
dc.description.abstractStrains of Escherichia coli may exist as a beneficial human commensal or a pathogen capable of causing morbidity and mortality. Of the E. coli which causes human disease, many strains which cause bacteremia have been identified as possessing virulence factors which make them more resistant to the complement system. The bacterial amyloid fibril, curli, functions in bacterial adherence and the formation of biofilm. Curli-producing parental and curli-deficient mutant E. coli was compared in its survival to human complement, using in vitro serum sensitivity assays. Results showed an increase in the survival of curli-producing E. coli, which suggested that curli defends against complement killing. An in vivo murine model of E. coli-induced sepsis demonstrated that curli-producing bacteria also survived significantly better in the blood of mice. Immunostaining and flow cytometry was done to determine if parental and mutant strains of E. coli differentially bind to complement components C1q and C3. Results demonstrated that curli increases binding of C1q, but does not affect C3 binding. Blocking the classical pathway suggested that, in these assays, the classical pathway was the major contributor to complement activation and curli inhibits its activity. In addition, blocking the alternative pathway supported that the classical pathway was the main mechanism for complement activation and suggested that curli is not involved in protecting E. coli against alternative pathway activation. Results of this study conclude that curli defends E. coli against complement killing via inhibition of the classical complement pathway.
dc.format.extent72 pages
dc.language.isoeng
dc.publisherTemple University. Libraries
dc.relation.ispartofTheses and Dissertations
dc.rightsIN COPYRIGHT- This Rights Statement can be used for an Item that is in copyright. Using this statement implies that the organization making this Item available has determined that the Item is in copyright and either is the rights-holder, has obtained permission from the rights-holder(s) to make their Work(s) available, or makes the Item available under an exception or limitation to copyright (including Fair Use) that entitles it to make the Item available.
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/
dc.subjectMicrobiology
dc.subjectImmunology
dc.subjectComplement System
dc.subjectEscherichia Coli
dc.titleTHE ROLE OF BACTERIAL AMYLOID FIBRILS IN ESCHERICHIA COLI COMPLEMENT RESISTANCE
dc.typeText
dc.type.genreThesis/Dissertation
dc.contributor.committeememberPiggot, Patrick
dc.contributor.committeememberButtaro, Bettina A.
dc.description.departmentMicrobiology and Immunology
dc.relation.doihttp://dx.doi.org/10.34944/dspace/780
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
dc.description.degreeM.S.
refterms.dateFOA2020-10-20T13:33:35Z


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