Thesis (M.S.)--Brigham Young University. Dept. of Microbiology and Molecular Biology, 2007. / Includes bibliographical references (p. 55-61).

Thesis (Ph. D.)--University of Alabama at Birmingham, 2009. / Additional advisors: Bill J. Baker, James B. McClintock, Donald D. Muccio, Robert W. Thacker. Description based on contents viewed June 3, 2009; title from PDF t.p. Includes bibliographical references.

Thesis (Ph. D.)--University of Chicago, Dept. of Ecology and Evolution. / Includes bibliographical references. Also available on the Internet.

Thesis (doctoral)--Nijmegen, 1984.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1968. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph. D.)--University of Florida, 2004. / Typescript. Title from title page of source document. Document formatted into pages; contains 149 pages. Includes vita. Includes bibliographical references.

Thesis (Ph. D. in Microbiology and Immunology)--Vanderbilt University, May 2007. / Title from title screen. Includes bibliographical references.

This thesis reports investigations of the interactions between the intestinal epithelial barrier and the intracellular apicomplexan Eimeria spp., both in vivo and in vitro. Initially, conventional in vivo studies using genetically modified animals were used to investigate the contribution of innate lymphoid cells (ILCs) to immune protection of the intestinal barrier. Additionally, to understand complex epithelial host-pathogen interactions a novel in vitro model of small intestine organoids was developed. Data suggest that immunoprotection against Eimeria vermiformis infections is mediated by T cells. Furthermore, there is an indication that ILCs have a detrimental effect in Eimeria vermiformis-infected immunocompromised animals. However, the role for ILCs in the regulation of the immune response remains unclear. The life cycles of Eimeria vermiformis and Eimeria falciformis are highly complex, comprising multiple schizogonies followed by a gametogony. In vitro life cycle completion has not been achieved to date due to the limitations of monolayer cell line models. It is likely that for a successful parasite development the interaction of the different epithelial cell types present in intestinal organoids is required. The development of intestinal organoids by Sato and colleagues gave rise to a breakthrough in cellular studies, providing the tools to study complex interactions between host tissues and invading pathogens in vitro. I showed that small intestine-derived organoids grow exponentially after passage and that each organoid contains distinct specialised epithelial cell types, such as Paneth, Goblet or enteroendocrine cells, suggesting that the organoid model closely resembles the native intestinal epithelium and that Eimeria spp. benefit from the three-dimensional structure and physiological characteristics of the organoid model. Intestinal organoids were infected with E. vermiformis or E. falciformis sporozoites. These completed several rounds of asexual replication but did not proceed to the final gametogony. Despite the need for the development of sensitive techniques applicable to three-dimensional cell culture models, these results indicate that intestine-derived organoids are a promising model to study host-parasite interactions at the intestinal epithelial barrier at the cellular and molecular levels.

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