Date of Award

4-30-2024

Degree Type

Thesis

Degree Name

Master of Science (MS)

Department

Microbiology and Immunology

First Advisor

Dorothy Sojka

Abstract

Following parturition, the uterus must undergo significant changes in size and structure through a process called postpartum remodeling. This process is known to have both pro- and anti- inflammatory components. However, how various immune cells contribute to remodeling and the pathways that promote inflammation are not well understood. We hypothesize that immune cells that infiltrate the uterus postpartum modulate inflammation to promote postpartum remodeling. Our preliminary data suggests that inflammatory cell death may contribute to the inflammation present in the early postpartum period, and thus further studies will analyze caspase-1, gasdermin D, and IL-1β and IL-18. To analyze the immune compartment of the postpartum uterus under normal and infection-like conditions, we will use high dimensional flow cytometry. Our preliminary data shows an influx (or expansion) of natural killer (NK) cells in the uterus following delivery. NK cells are the most abundant lymphocyte at the maternal-fetal interface in early to mid-pregnancy, but their numbers decline significantly in late pregnancy. The timely arrival of NK cells following parturition leads us to hypothesize that they may play a role in remodeling the postpartum uterus. To determine how the absence of lymphocyte populations affects the overall immune microenvironment of the uterus, we will utilize Rag2-/-il2rg-/- (Ragγc) mice. We hypothesize that these mice will have impaired postpartum remodeling and diminished fertility with each pregnancy, which we will assess through six-month breeding studies, flow cytometry, and histological analysis. We aim to understand how physiological inflammation is generated and controlled during postpartum remodeling and how that inflammation is altered under infection-like conditions.

Available for download on Sunday, July 12, 2026

Included in

Microbiology Commons

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