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Characterizing the Involvement of Ocular Glands and Stromal Fibroblasts in Corneal Infections.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Characterizing the Involvement of Ocular Glands and Stromal Fibroblasts in Corneal Infections./
作者:	Montgomery, Micaela.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2021,
面頁冊數:	165 p.
附註:	Source: Dissertations Abstracts International, Volume: 82-12, Section: B.
Contained By:	Dissertations Abstracts International82-12B.
標題:	Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28414350
ISBN:	9798515281908

Characterizing the Involvement of Ocular Glands and Stromal Fibroblasts in Corneal Infections.
Montgomery, Micaela.

Characterizing the Involvement of Ocular Glands and Stromal Fibroblasts in Corneal Infections. - Ann Arbor : ProQuest Dissertations & Theses, 2021 - 165 p.

Source: Dissertations Abstracts International, Volume: 82-12, Section: B.

Thesis (Ph.D.)--The University of Oklahoma Health Sciences Center, 2021.

This item must not be sold to any third party vendors.

Over 2 million people worldwide experience corneal infections every year. The resulting pathology from these infections can cause chronic deficits in vision and overall eye health. A variety of pathogens have been found to cause keratitis, including viruses, bacteria, fungi, and parasites. The full impact of these infections on the ocular glands and the cornea are not fully understood. This dissertation describes the involvement of ocular glands and stromal fibroblasts in several infection models. First, we found that ocular glands became infected with HSV-1 secondary to an initial corneal infection and also experienced a dramatic influx of immune cells. Similarly, we found glands became infected following Pseudomonas aeruginosa keratitis. We observed that removal of these glands prior to HSV-1 infection altered corneal disease course, with increased viral load and decreased immune cell infiltration. Despite corneal infection resolving, ocular glands had altered eicosanoid expression, suggesting prolonged inflammation following infection. Second, we established a new model for assessing fungal-fibroblast interactions during fungal keratitis in which human stromal fibroblasts produce extracellular matrix and form a 3D environment similar to an actual cornea stroma. We validated that fibroblasts in our model could respond to fungal infection and captured novel images of fibroblasts physically interacting with Fusarium petroliphilum conidia. Aspergillus fumigatus expressed higher levels of dppIV and dppV, protease genes in our model compared to plain Eagles Minimal Essential Media conditions, likely due to the absence of nutrients in our PBS-only inoculum. Overall, the findings in this dissertation improve our understanding of how different players in the ocular environment contribute to keratitis disease pathology.

ISBN: 9798515281908Subjects--Topical Terms:

536250
Microbiology.
Subjects--Index Terms:

Cornea

Characterizing the Involvement of Ocular Glands and Stromal Fibroblasts in Corneal Infections.
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520 $a Over 2 million people worldwide experience corneal infections every year. The resulting pathology from these infections can cause chronic deficits in vision and overall eye health. A variety of pathogens have been found to cause keratitis, including viruses, bacteria, fungi, and parasites. The full impact of these infections on the ocular glands and the cornea are not fully understood. This dissertation describes the involvement of ocular glands and stromal fibroblasts in several infection models. First, we found that ocular glands became infected with HSV-1 secondary to an initial corneal infection and also experienced a dramatic influx of immune cells. Similarly, we found glands became infected following Pseudomonas aeruginosa keratitis. We observed that removal of these glands prior to HSV-1 infection altered corneal disease course, with increased viral load and decreased immune cell infiltration. Despite corneal infection resolving, ocular glands had altered eicosanoid expression, suggesting prolonged inflammation following infection. Second, we established a new model for assessing fungal-fibroblast interactions during fungal keratitis in which human stromal fibroblasts produce extracellular matrix and form a 3D environment similar to an actual cornea stroma. We validated that fibroblasts in our model could respond to fungal infection and captured novel images of fibroblasts physically interacting with Fusarium petroliphilum conidia. Aspergillus fumigatus expressed higher levels of dppIV and dppV, protease genes in our model compared to plain Eagles Minimal Essential Media conditions, likely due to the absence of nutrients in our PBS-only inoculum. Overall, the findings in this dissertation improve our understanding of how different players in the ocular environment contribute to keratitis disease pathology.
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