Event Title

Helminth Parasites Protect from Intestinal Damage in Mice Model of IBD

Location

CSU Ballroom

Start Date

11-4-2017 10:00 AM

End Date

11-4-2017 11:30 AM

Student's Major

Biological Sciences

Student's College

Science, Engineering and Technology

Mentor's Name

Allison Land

Mentor's Department

Biological Sciences

Mentor's College

Science, Engineering and Technology

Second Mentor's Name

Natalie Gooder

Second Mentor's Department

Biological Sciences

Second Mentor's College

Science, Engineering and Technology

Description

Developed countries have seen a noticeable rise in allergic and autoimmune disease, but interestingly, less developed countries, which have low incidences of allergic and autoimmune disease, have high incidences of parasitic infections. A major part of an immune response is the balance between an inflammatory response and a regulatory response. Once the inflammatory response is triggered, the body induces phagocytes to migrate to the site of the foreign invader. Once at the site, phagocytes are activated and produce cytokines, which activate other cells in the immune system. Once an infection is detected and cytokines are activated, Tregs (regulatory T cells) control which cytokines are used and how. Inflammatory Bowel Disease (IBD) is an example of an autoimmune disease where we see a damaging inflammatory response. I hypothesize that parasites may be used to trick the immune system into shutting off inflammation in IBD. Using a well-established IBD mouse model, heat-killed parasites (or a control) will be fed to the mice. The ability of the parasites to modulate the immune response in IBD will be assessed by measuring IL- 10 (anti-inflammatory) and IFNγ (pro-inflammatory) cytokines using an ELISA. I anticipate that the ability to protect mice from intestinal damage will be shown by an increase in IL-10 (anti-inflammatory) and a decrease in IFNγ (pro-inflammatory). These findings will demonstrate the ability of heat-killed parasites to stimulate an anti-inflammatory immune response, protecting against chronic inflammation. This would provide novel insight into lessening symptoms of IBD and other autoimmune diseases.

This document is currently not available here.

Share

COinS
 
Apr 11th, 10:00 AM Apr 11th, 11:30 AM

Helminth Parasites Protect from Intestinal Damage in Mice Model of IBD

CSU Ballroom

Developed countries have seen a noticeable rise in allergic and autoimmune disease, but interestingly, less developed countries, which have low incidences of allergic and autoimmune disease, have high incidences of parasitic infections. A major part of an immune response is the balance between an inflammatory response and a regulatory response. Once the inflammatory response is triggered, the body induces phagocytes to migrate to the site of the foreign invader. Once at the site, phagocytes are activated and produce cytokines, which activate other cells in the immune system. Once an infection is detected and cytokines are activated, Tregs (regulatory T cells) control which cytokines are used and how. Inflammatory Bowel Disease (IBD) is an example of an autoimmune disease where we see a damaging inflammatory response. I hypothesize that parasites may be used to trick the immune system into shutting off inflammation in IBD. Using a well-established IBD mouse model, heat-killed parasites (or a control) will be fed to the mice. The ability of the parasites to modulate the immune response in IBD will be assessed by measuring IL- 10 (anti-inflammatory) and IFNγ (pro-inflammatory) cytokines using an ELISA. I anticipate that the ability to protect mice from intestinal damage will be shown by an increase in IL-10 (anti-inflammatory) and a decrease in IFNγ (pro-inflammatory). These findings will demonstrate the ability of heat-killed parasites to stimulate an anti-inflammatory immune response, protecting against chronic inflammation. This would provide novel insight into lessening symptoms of IBD and other autoimmune diseases.

Recommended Citation

Helmer, Shannon. "Helminth Parasites Protect from Intestinal Damage in Mice Model of IBD." Undergraduate Research Symposium, Mankato, MN, April 11, 2017.
http://cornerstone.lib.mnsu.edu/urs/2017/poster-session-A/10