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DC Field | Value | Language |
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dc.contributor.advisor | MacNeil, Lesley | - |
dc.contributor.author | DiBernardo, Mercedes | - |
dc.date.accessioned | 2022-01-27T19:04:37Z | - |
dc.date.available | 2022-01-27T19:04:37Z | - |
dc.date.issued | 2021 | - |
dc.identifier.uri | http://hdl.handle.net/11375/27320 | - |
dc.description.abstract | Commensal microorganisms that colonize host surfaces can modulate susceptibility to infection. This can occur through direct inhibition of pathogen growth via competitive exclusion, or by modulation of the host environment to prevent pathogen dissemination and infection-mediated damage. However, understanding the mechanisms underlying these interactions is challenging due to the complexity of the human microbiome. The model organism Caenorhabditis elegans allows for the study of individual host-microbiota interactions, given they are bacterivorous and can be maintained monoxenically on a bacterial strain of interest. Here, we investigate the influence of human respiratory tract microbiota isolates on C. elegans susceptibility to Pseudomonas aeruginosa infection. Identifying isolates that differentially regulate resistance to infection will provide insight into how particular strains isolated from the human microbiome may act synergistically with P. aeruginosa or improve infection outcomes. A screen of isolates derived from the human respiratory tract was carried out using a liquid-based P. aeruginosa infection assay. Animals were first exposed to individual microbiotal isolates during development, prior to infection with a pathogenic strain of P. aeruginosa, PA14. This screen identified two non-pathogenic isolates of P. aeruginosa that increased survival during PA14 liquid killing, compared to animals pre-exposed to E. coli OP50. This protective phenotype was also induced by other mildly pathogenic strains of P. aeruginosa, including a laboratory strain with genetically attenuated virulence, PAO1 ∆vfr, as well as the pathogen Salmonella enterica. This work details the bacterial factors and host pathways that may regulate S. enterica and P. aeruginosa-mediated protection from PA14 liquid killing. | en_US |
dc.language.iso | en | en_US |
dc.title | Exploring resistance to Pseudomonas aeruginosa infection in Caenorhabditis elegans | en_US |
dc.type | Thesis | en_US |
dc.contributor.department | Biochemistry and Biomedical Sciences | en_US |
dc.description.degreetype | Thesis | en_US |
dc.description.degree | Master of Science (MSc) | en_US |
dc.description.layabstract | The human microbiome is the collection of beneficial bacteria that live on and in the human body and are involved in maintaining health in a number of ways, such as protecting from infection by pathogenic bacteria. In this work, we investigate the role the human microbiome has on altering the severity of an infection. Here, we use the model organism Caenorhabditis elegans, a microscopic roundworm that can be infected and killed by many of the same bacterial pathogens that infect humans. This worm model is particularly beneficial to use for this project because they grow and die more rapidly than other animals used to study infection, facilitating the ability to identify protective species within a large collection of bacterial isolates. This study shows that microbially-produced vitamins play an important role in enhancing survival during an infection. By studying infection resistance in model organisms such as C. elegans, we can identify factors that may also be important in regulating resistance to infection in humans. | en_US |
Appears in Collections: | Open Access Dissertations and Theses |
Files in This Item:
File | Description | Size | Format | |
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DiBernardo_Mercedes_A_2021December_MSc.pdf | 2.08 MB | Adobe PDF | View/Open |
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