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dc.contributor.authorBarber, Ellen M.
dc.identifier.citationSource: Dissertation Abstracts International, Volume: 65-09, Section: B, page: 4357.;Advisors: Jeffrey W. Pollard.
dc.description.abstractIt is still unknown precisely how a successful pregnancy is maintained given the potential of the mother's immune system for rejecting the allogenic fetus. There is a growing amount of evidence to support the idea that immune responses are precisely regulated at this interface, creating a unique immunologic environment. This regulation becomes even more important when infections at this anatomic location elicit a maternal immune response that could threaten the immunological balance needed to protect the fetus. This thesis describes studies of the immune response at the maternal-fetal interface using pregnant mice infected with the gram positive bacterium Listeria monocytogenes , that has a predilection for growth in the decidua basalis of the murine placenta.;Work from this laboratory has ascribed a function for the fetally derived trophoblastic cells of the placenta in recruiting neutrophils to sites of L. monocytogenes infection in the placenta. Since macrophages are excluded from the murine utero-placental unit, neutrophils are the major early immune mediator against L. monocytogenes infection at this site. The cytokines Interferon-gamma (IFN-gamma) and Tumor Necrosis Factor-alpha (TNF-alpha) are necessary for a successful immune response to systemic Listerial infection. We have shown that these cytokines are induced at the maternal fetal interface upon L. monocytogenes infection and hypothesize that they may also play an important role for clearing placental infection.;Utilizing mice carrying null mutations for TNF-alpha and IFN-gamma and their receptors, work thus far has shown that Listerial titers in placentae are significantly increased in the absence of either of these signaling pathways. Genetic crosses have also revealed that the major source of these cytokine is maternal, not fetal and that the cells responding to these cytokies during infection are also of a maternal origin. Current studies are aimed at characterizing the cellular location of these cytokines and their receptors during L. monocytogenes infection.;We have shown that maternal stromal cells of the metrial gland and decidua basalis produce indoleamine 2,3-dioxygenase (IDO) an enzyme that is known to suppress the growth of T cells and some pathogenic bacteria via its metabolism of tryptophan. IDO levels increase in the placenta in response to L. monocytogenes infection and this is dependant upon IFN-gamma. (Abstract shortened by UMI.).
dc.publisherProQuest Dissertations & Theses
dc.subjectAnimal Physiology.
dc.subjectMolecular biology.
dc.titleRegulation of the immune response to Listeria monocytogenes infection in the murine placenta

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