Steven Mangold
Pronouns:
Research Mentor(s): Catherine Ptaschinski
Research Mentor School/College/Department: Pathology / Medicine
Program: UROP
Session: Session 2 (10:00am – 10:50am)
Authors: Steven Mangold, Nicholas Lukacs, Catherine Ptaschinski
Abstract
In the United States, anaphylaxis from food allergies results in over 30,000 hospitalizations yearly. Reactions to allergens by the immune system are dependent on a number of factors, including the permeability of barrier cells of the small intestine. Leaky barriers can expose the intestine to more protein, which can subsequently cause more severe reactions. A leaky barrier can be characterized by the lack of Junctional Adhesion Molecule-A (JAM-A), a protein that is known to have a significant role in barrier stability. We wanted to look at how mice with leaky intestinal barriers differed from mice with normal barrier function at baseline levels, prior to exposure to allergens. In doing so, we took samples of intestinal tissues from these mice, and analyzed the levels of expression in certain genes involved in driving or suppressing an allergic response. The groups of mice studied consisted of: mice with normal barrier function (Wild-Type), mice lacking JAM-A protein (KO) entirely, and mice with targeted knock-out JAM-A in the small intestine. Mice with the targeted KO were created using Cre-lox recombinase technology. We also looked at differences between males and females within the same grouping. We found no differences in inflammatory genes in mice with a leaky barrier, but did see changes in immunosuppressive genes, including differences between males and females. These differences in suppressive genes may contribute to the increased anaphylactic response in mice with a leaky barrier.
