Date Available
5-8-2014
Year of Publication
2014
Document Type
Master's Thesis
Degree Name
Master of Science in Medical Sciences (MSMS)
College
Medicine
Department/School/Program
Microbiology, Immunology, and Molecular Genetics
Advisor
Dr. Sarah D'Orazio
Abstract
The invasive pathways, InlA- and InB-mediated uptake and M cell transcytosis, that Listeria monocytogenes uses to invade the intestine have mainly been studied using infection models that do not truly replicate what occurs during a natural infection. Recently, our lab has developed an oral infection model that is more physiolocally relevant to what occurs during food borne listeriosis. We have sought to evaluate the relative roles of the previously defined invasive pathways, in our oral model of infection. We have done this by utilizing an InlAmCG Lm strain that is able to bind murine E-cadherin, knockout Lm strains, ΔinlA Lm, and ΔinlAΔinlB Lm. We also took advantage of a knockout mice strain CD137-/-that has M cells that are deficient in M cell transcytosis. We were able to show that these invasive pathways are relevant in our oral infection model, that M cell transcytosis is a compensatory pathway for InlA-mediated uptake, and that there might be another mechanism that L. monocytogenes uses to invade the intestines. To confirm this, it is necessary though that the M cell transcytosis deficiency be confirmed in the CD137-/- mice.
Recommended Citation
Denney, Hilary, "Listeria Monocytogenes can Utilize both M Cell Transcytosis and InlA-Mediated Uptake to Cross the Epithelial Barrier of the Intestine during an Oral Infection Model of Listeriosis" (2014). Theses and Dissertations--Medical Sciences. 3.
https://uknowledge.uky.edu/medsci_etds/3
Included in
Bacteria Commons, Bacterial Infections and Mycoses Commons, Bacteriology Commons, Medical Microbiology Commons, Other Microbiology Commons, Pathogenic Microbiology Commons
