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dc.contributor.advisorWhelan, Kelly A.
dc.creatorHall, Timothy Michael
dc.date.accessioned2020-11-04T15:19:57Z
dc.date.available2020-11-04T15:19:57Z
dc.date.issued2019
dc.identifier.urihttp://hdl.handle.net/20.500.12613/2969
dc.description.abstractEosinophilic esophagitis (EoE) is a chronic allergic pathology of the esophagus characterized by infiltration of eosinophils into the esophageal mucosa. EoE results in considerable impact on patient quality of life, substantiating the need to better understand the pathobiology of the disease in order to define novel approaches to diagnosis, monitoring and therapy. Our previous studies indicate an increase in circulating mitochondrial DNA in patients with active EoE and extracellular structures consistent with mitochondria in esophageal epithelium of patients with active EoE inflammation. While published studies provide evidence of a genetic link between mitochondrial dysfunction and development of EoE, the functional role of mitochondria in EoE pathophysiology remains unclear. In this thesis, we use immunohistochemistry on human patient biopsies, mouse models of EoE-like inflammation, and complementary in vitro and ex vivo models to explore the effects of the EoE inflammatory milieu on mitochondria in esophageal keratinocytes. We report that mitochondrial content is increased in human patients and mice with EoE inflammation. We also provide evidence that the EoE-associated cytokine, interleukin-13 increases mitochondrial DNA level and mitochondrial activity in vitro. To explore the role of autophagy in mitochondrial regulation in esophageal keratinocytes, we began generation of an autophagy-deficient cell line. This thesis provides foundation for further studies evaluating the role and mechanisms of mitochondrial regulation in the context of eosinophilic esophagitis.
dc.format.extent84 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.subjectBiology
dc.titleEXPLORING THE MECHANISMS OF ESOPHAGEAL KERATINOCYTE HOMEOSTASIS IN THE CONTEXT OF EOSINOPHILIC ESOPHAGITIS
dc.typeText
dc.type.genreThesis/Dissertation
dc.contributor.committeememberHaines, Dale
dc.contributor.committeememberTempera, Italo
dc.description.departmentBiomedical Sciences
dc.relation.doihttp://dx.doi.org/10.34944/dspace/2951
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.dateFOA2020-11-04T15:19:57Z


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