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T cell independent mechanisms for protection against Mycobacterium tuberculosis infection

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dc.contributor.authorBickett, Thomas, author
dc.contributor.authorIzzo, Angelo, advisor
dc.contributor.authorDow, Steven, committee member
dc.contributor.authorMcLean, Jennifer, committee member
dc.contributor.authorBowen, Richard, committee member
dc.contributor.authorArgueso, Lucas, committee member
dc.date.accessioned2019-09-10T14:36:24Z
dc.date.available2019-09-10T14:36:24Z
dc.date.issued2019
dc.description.abstractThe live attenuated Mycobacterium bovis strain Bacille Calmette Guérin (BCG) is a potent innate immune stimulator. Innate Immunity provides the host with the ability to immediately respond to invasion by pathogens and can be utilized through the use of molecular adjuvants to trigger specific innate mechanisms leading to adaptive immunity. In the C57BL/6 mouse model of tuberculosis, BCG stimulated immunity causes a significant reduction of M. tuberculosis burden after pulmonary infection. Our studies indicate that BCG induced protection against pulmonary M. tuberculosis through early monocyte recruitment is present as early as 7 days after vaccination. This protection showed longevity, as it did not wane when mice were infected 30 days post vaccination. As BCG induced mycobacterial killing after 7 days, we sought to identify the contribution of different innate immune components to better understand mechanisms required for mycobacterial killing. When BCG was administered through subcutaneous inoculation, we found that there was significant monocyte recruitment in the lungs within 7 days after vaccination. Further studies revealed that killing of mycobacterium is dependent on BCG being viable and is monocyte derived, independent of trained innate immunity, highlighting a novel mechanism for killing M. tuberculosis. With the rise of drug resistant strains of Mycobacterium tuberculosis, new vaccine development is paramount. A better understanding of the BCG vaccine will hopefully lead to the development of a more effective alternative.
dc.format.mediumborn digital
dc.format.mediumdoctoral dissertations
dc.identifierBickett_colostate_0053A_15631.pdf
dc.identifier.urihttps://hdl.handle.net/10217/197402
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.subjectinnate immunity
dc.subjecttrained innate immunity
dc.subjecttuberculosis
dc.subjectmacrophage
dc.subject.lcshBCG
dc.titleT cell independent mechanisms for protection against Mycobacterium tuberculosis infection
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.disciplineCell and Molecular Biology
thesis.degree.grantorColorado State University
thesis.degree.levelDoctoral
thesis.degree.nameDoctor of Philosophy (Ph.D.)

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