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Title page for ETD etd-03172016-151927

Type of Document Dissertation
Author Petersen, Christine Pope
URN etd-03172016-151927
Title Inflammatory Mediators promote the development and progression of metaplasia in the stomach
Degree PhD
Department Cell and Developmental Biology
Advisory Committee
Advisor Name Title
David Bader Committee Chair
James Goldenring Committee Chair
Barbara Fingleton Committee Member
Chin Chiang Committee Member
Robert Coffey Committee Member
  • cytokines
  • metaplasia
  • inflammation
  • gastric
  • stomach
  • M2 macrophages
  • macrophages
  • SPEM
Date of Defense 2016-02-08
Availability unrestricted
Spasmolytic polypeptide-expression metaplasia (SPEM) develops in the atrophic stomach and progresses to an intestinalized SPEM in the setting of inflammation. Different immune deficient mouse models determined that T-cells, B-cells, IFN gamma and neutrophils are not essential for the progression to an intestinalized SPEM. However, studies using macrophage-depleted mice found that specifically M2 macrophages were necessary for SPEM to become intestinalized. Efforts to understand macrophage-derived factors that promote the advancement of metaplasia led to RNA-sequencing of gastric macrophages in the setting of SPEM and intestinalized SPEM. A novel profile of activated gastric macrophages revealed that IL-33 is significantly upregulated in the setting of intestinalized SPEM. Inducing parietal cell loss in IL33 knock out mice uncovered an essential role for IL-33 in the transdifferentiation of mature chief cells into SPEM cells. Furthermore, IL-33 is required for the polarization of recruited macrophages towards M2a. Thus establishing a vital role for IL-33 in the development of metaplasia and macrophage polarization in response to acute parietal cell loss in the stomach.
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