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dc.contributor.advisorJohnson, Natalie M
dc.contributor.advisorRodrigues Hoffmann, Aline
dc.creatorLau, Carmen
dc.date.accessioned2023-02-07T16:03:35Z
dc.date.available2024-05-01T06:06:24Z
dc.date.created2022-05
dc.date.issued2022-01-20
dc.date.submittedMay 2022
dc.identifier.urihttps://hdl.handle.net/1969.1/197117
dc.description.abstractDespite increasing movements towards cleaner air regulations, air pollution remains a critical factor in millions of deaths globally every year. Particulate matter (PM) is one of the many types of air pollution, and ultrafine particulate matter (UFP) is the highly detrimental and under-regulated smallest fraction of PM. While it is known that PM exposure during pregnancy can lead to harmful neonatal effects, such as stillbirth and low birth weight, little literature exists on the specific effects that UFPs may have during this critical time window. Prenatal PM exposure has also been shown to significantly increase the risk of the infant developing asthma or respiratory infections during childhood, and it is likely, though not confirmed, that UFPs would likely do the same. We undertook to develop a murine model of prenatal UFP exposure, to examine how it might alter neonate’s ability to combat respiratory infection, and to examine the possible mechanisms by which prenatal UFPs might exert its influence through the dam to the fetus. This last goal was accomplished by looking at the effect that Nrf2, a major transcription factor controlling antioxidant responses, may play in the neonatal response to UFP exposure. Our findings demonstrated that prenatal UFP exposure did enhance the severity of neonatal respiratory disease, specifically to respiratory syncytial virus (RSV). When examining neonates only exposed to UFPs prenatally, we found that Nrf2 deficient neonates had a reduced ability to respond to oxidative stress than their wildtype counterparts, and that their pulmonary T cell populations had significantly increased levels of Th1 and Th2 immune cells when stimulated by UFPs. This suggests that prenatal UFPs may exert their influence by oxidative stress, perhaps transferred from the mother, and by altering pulmonary T cell differentiation and potential priming for neonatal respiratory infections. Overall, our research shows that UFPs exert negative influences on fetal health that have an impact in the neonatal period, thus demonstrating a need for increased regulation and public health preventative measures to protect the health of mothers and children in highly polluted regions.
dc.format.mimetypeapplication/pdf
dc.language.isoen
dc.subjectultrafine particulate matter
dc.subjectrespiratory disease
dc.subjectmouse model
dc.subjectNrf2
dc.titleThe Role of Ultrafine Particulate Matter and Nrf2 in the Pathogenesis of Neonatal Respiratory Syncytial Virus Disease at Texas A&M University
dc.typeThesis
thesis.degree.departmentVeterinary Pathobiology
thesis.degree.disciplineBiomedical Sciences
thesis.degree.grantorTexas A&M University
thesis.degree.nameDoctor of Philosophy
thesis.degree.levelDoctoral
dc.contributor.committeeMemberCannon, Carolyn
dc.contributor.committeeMemberCriscitiello, Michael
dc.type.materialtext
dc.date.updated2023-02-07T16:03:36Z
local.embargo.terms2024-05-01
local.etdauthor.orcid0000-0002-1993-6373


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