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Understanding Mycobacterium abscessus in cystic fibrosis mice

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dc.contributor.authorVongtongsalee, Kridakorn, author
dc.contributor.authorOrdway, Diane, advisor
dc.contributor.authorSchenkel, Alan, committee member
dc.contributor.authorChatterjee, Delphi, committee member
dc.contributor.authorKirby, Michael, committee member
dc.date.accessioned2019-06-14T17:06:31Z
dc.date.available2019-06-14T17:06:31Z
dc.date.issued2019
dc.description.abstractCystic fibrosis (CF) is caused by mutation of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene, which normally encodes an ABC transporter-class ion channel protein that allows chloride and thiocyanate ions transport across epithelial cell membranes. Thus, CFTR plays an important role in airway homeostasis. Mutations of CFTR in patients with CF leads to a defect in transport of chloride and thiocyanate ions by epithelial cells, resulting in a multi-system disorder that affects the respiratory tract, gastrointestinal tract, the endocrine system, among others. The epithelial cell dysfunction in the lungs of CF patients also leads to an impaired pulmonary defense mechanism, resulting in decreased bacterial clearance and chronic inflammation. In CF patients, lung disease due to non-tuberculous mycobacteria (NTM) — an environmental organisms found in soil, water, and biofilms — is one of the most feared complications. Among the NTM, the rapidly-growing Mycobacterium abscessus is particularly notorious given its intrinsic resistance to many antibiotics. The transmission of M. abscessus to humans occurs by wound contamination, airborne transmission, or ingestion. Despite the fact that M. abscessus infection is increasing worldwide, little is known about how M. abscessus causes disease. To improve our understanding of M. abscessus in CF patients, we set out to investigate the progression of M. abscessus infection in a CF mouse model by developing a reinfection mouse model using three different strains of "CF mouse" — Beta-ENaC mice, Cftrtm1UNCTgN(FABPCFTR) mice and CFTRtm1UNC/ CFTRtm1UNC mice — to track the bacterial burden and organ pathology. Our results support the hypothesis that repeated infection with M. abscessus is more likely to result in disease progression and increased pathogenesis of the disease in CF mouse models. The high bacterial burden persisted in the lung after four infections in β-ENaC transgenic mice and CFTRtm1UNC/CFTRtm1UNC mice and maintained in the organs by day 30. Cftrtm1UNCTgN(FABPCFTR) mice tended to show slowly increasing bacterial burden in all organs. In summary, we demonstrate that reinfection of the CF mouse models with M. abscessus is more likely to result in a sustained infection in the lungs associated with increased pulmonary pathology.
dc.format.mediumborn digital
dc.format.mediummasters theses
dc.identifierVongtongsalee_colostate_0053N_15397.pdf
dc.identifier.urihttps://hdl.handle.net/10217/195355
dc.languageEnglish
dc.language.isoeng
dc.publisherColorado State University. Libraries
dc.relation.ispartof2000-2019
dc.rightsCopyright and other restrictions may apply. User is responsible for compliance with all applicable laws. For information about copyright law, please see https://libguides.colostate.edu/copyright.
dc.titleUnderstanding Mycobacterium abscessus in cystic fibrosis mice
dc.typeText
dcterms.rights.dplaThis Item is protected by copyright and/or related rights (https://rightsstatements.org/vocab/InC/1.0/). You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s).
thesis.degree.disciplineMicrobiology, Immunology, and Pathology
thesis.degree.grantorColorado State University
thesis.degree.levelMasters
thesis.degree.nameMaster of Science (M.S.)

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