Javier Castro-Corral
Pronouns: He/Him
Research Mentor(s): Erin Janssen
Research Mentor School/College/Department: Pediatrics / Medicine
Program:
Authors:
Session: Session 2: 10:00 am – 10:50 am
Poster: 51
Abstract
Inflammatory bowel disease (IBD) is very common in the US affecting over 1.6 million people. A better understanding of the genetic factors contributing to IBD is an essential role for optimizing treatment in the future. We identified a young girl with early onset IBD. She has a homozygous coding variant (p.C588Y) in the CIAP2 gene, CIAP2 plays an essential role in innate cell signaling. In our study, we generated mice with the same homozygous variant in Ciap2 – Ciap2C586Y/C586Y. Studying these mice will allow us to determine if abnormal signaling through CIAP2 contributes to the development of IBD. We utilized a common model of colitis – treatment of mice with dextran sulfate sodium (DSS). Colitis is induced by adding DSS to the mouse’s drinking water. Using this model, we are able to observe any differences in DSS-induced colitis in wild-type mice compared to those that with the Ciap2 mutation. The study surprisingly found that the Ciap2C586Y/C586Y mice were more resistant to DSS induced inflammation compared with wild-type mice. We observed that the Ciap2C586Y/C586Y mice had lost less weight then the wild-type mice and had decreased scores of colonic inflammation. Further studies will be directed towards determining if this protective effect is observed with other models of colitis.
