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    The Cytokine Response to Pathogen N. gonorrhoeae and Commensal N. elongata

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    Author
    Brown, Morgan Mackenzie
    Issue Date
    2017
    Advisor
    So, Magdalene
    
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    Publisher
    The University of Arizona.
    Rights
    Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
    Abstract
    The Neisseria genus is predominantly comprised of commensals that are asymptomatically carried by humans. The pathogens N. gonorrhoeae (Ngo) and N. meningitidis are often asymptomatically carried, yet are causative agents of gonorrhoeae and meningitis respectively. N. elongata (Nel) is a commensal of the nasopharynx, and the most evolutionarily distal commensal to Ngo. It is unknown what factors drive commensal versus pathogenic lifestyle. All Neisseria contain genes for the Type IV Pilus, a retractile appendage important for modulating Ngo-host interactions. Ngo pilus retraction stimulates a cytoprotective environment that promotes Ngo carriage and host cell survival. Nel also express functional pili, but it is unknown if or how retraction is implicated in Nel-host interactions. Here we investigate how commensal Nel and pathogen N. gonorrhoeae differentially modulate the host via pilus retraction. We show that Nel pilus retraction is implicated in adherence and invasion of host cells, similar to Ngo. Nel pilus retraction stimulates a cytokine environment that is distinct from Ngo in vitro. This cytokine environment is maintained via EGFR and DUSP-1 signaling. We conclude that Nel pilus retraction is important for tuning the host-cell response to Nel carriage, and may promote a pro-commensal cytokine environment.
    Type
    text
    Electronic Thesis
    Degree Name
    B.S.
    Degree Level
    bachelors
    Degree Program
    Honors College
    Microbiology
    Degree Grantor
    University of Arizona
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    Honors Theses

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