Presentation Type

Poster Presentation

Abstract

Inflammatory bowel disease (IBD) is an autoimmune disorder where the immune system attacks healthy tissue. IBD can occur in both adults and children, describing Ulcerative Colitis (UC) and Crohn’s Colitis (CC). Our lab studies human alpha defensin 5 (HD5), an antimicrobial peptide that normally maintains small intestinal sterility. However, in CC patients, HD5 is overexpressed in the colon. Preliminary data suggests that HD5 increases colonic cell death. This project aims to determine if HD5 induces apoptosis and its mechanisms. To this end, we will test if the suppression of caspase enzymes with a pan-caspase inhibitor reduces cell death triggered by HD5. We will use the XTT assay to assess cell viability and Western blotting to detect caspase activation, avoiding autofluorescence issues that were encountered before. These methods will allow us to verify if HD5 triggers cellular death via caspase-dependent apoptotic pathways and which are affected. We expect that cellular apoptosis will be reduced upon treatment with both HD5 and the caspase inhibitor, and we hope to prove by Western blotting which caspases are activated by HD5. These findings will clarify HD5’s role in CC and its apoptotic effects on colonic epithelial cells. By using non-fluorescent techniques, we aim to eliminate some of the limitations seen in earlier studies and clarify the effects of HD5 in more detail. The results will provide new insights into the impact of HD5 on gastrointestinal health and inform future approaches to treating inflammatory bowel disease.

Faculty Mentor

Amanda D. Williams

Share

COinS
 

Understanding the role of HD5 in Colonic Epithelial Cell Death

Inflammatory bowel disease (IBD) is an autoimmune disorder where the immune system attacks healthy tissue. IBD can occur in both adults and children, describing Ulcerative Colitis (UC) and Crohn’s Colitis (CC). Our lab studies human alpha defensin 5 (HD5), an antimicrobial peptide that normally maintains small intestinal sterility. However, in CC patients, HD5 is overexpressed in the colon. Preliminary data suggests that HD5 increases colonic cell death. This project aims to determine if HD5 induces apoptosis and its mechanisms. To this end, we will test if the suppression of caspase enzymes with a pan-caspase inhibitor reduces cell death triggered by HD5. We will use the XTT assay to assess cell viability and Western blotting to detect caspase activation, avoiding autofluorescence issues that were encountered before. These methods will allow us to verify if HD5 triggers cellular death via caspase-dependent apoptotic pathways and which are affected. We expect that cellular apoptosis will be reduced upon treatment with both HD5 and the caspase inhibitor, and we hope to prove by Western blotting which caspases are activated by HD5. These findings will clarify HD5’s role in CC and its apoptotic effects on colonic epithelial cells. By using non-fluorescent techniques, we aim to eliminate some of the limitations seen in earlier studies and clarify the effects of HD5 in more detail. The results will provide new insights into the impact of HD5 on gastrointestinal health and inform future approaches to treating inflammatory bowel disease.

 

To view the content in your browser, please download Adobe Reader or, alternately,
you may Download the file to your hard drive.

NOTE: The latest versions of Adobe Reader do not support viewing PDF files within Firefox on Mac OS and if you are using a modern (Intel) Mac, there is no official plugin for viewing PDF files within the browser window.