Date Presented

Spring 5-2021

Document Type

Thesis

Degree Name

Bachelor of Science

Department

Biomedical Science

First Advisor

Dr. David Freier

Second Advisor

Dr. Jennifer Styrksy

Third Advisor

Dr. Priscilla Gannicott

Abstract

Celiac disease disrupts the intestinal mucosa when exposed to gliadin-containing grains. The immune system’s response to gliadin is an intricate molecular signaling cascade involving the adaptive and innate immune systems. A majority of the research in this area focuses upon the adaptive immune system; however, recent work suggests the innate immune system plays a significant role. Macrophages are innate immune system cells that work to protect a host organism from infection. RAW 264.7 Murine macrophages serve as a model for inflammatory responses by producing nitric oxide in response to an inflammatory stimulus. Experiments determined the level of macrophage activation from pepsin-trypsin digested gliadin (PT-gliadin) and undigested gliadin in comparison to an untreated control and a known stimulant, bacterial Lipopolysaccharide (LPS). Concentrations of PT-gliadin showed evidence of a dose-response effect with 100 ug/mL inducing a moderate stimulus and 500 and 1000 ug/mL stimulating a higher level of response. No significant differences were found between macrophage activation when exposed to either PT- gliadin or undigested gliadin. Determining the ability of gliadin to stimulate the RAW 264.7 macrophages will allow for the investigation of potential roles for macrophages in the inflammatory process induced by gliadin. Examining the effects of gliadin on macrophages can determine the involvement of the innate immune system, which can then extend to the connection between the innate and adaptive immune responses. Understanding this molecular cascade can lead to a more complete understanding of the immune response associated with Celiac Disease and other similar conditions induced by gluten and its molecular relatives.

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