Class
Article
College
College of Agriculture and Applied Sciences
Department
Animal, Dairy, and Veterinary Sciences Department
Faculty Mentor
Abby Benninghoff
Presentation Type
Poster Presentation
Abstract
Colorectal cancer (CRC) is the third most common cause of cancer death in the United States. Diet and gut microbiome have shown to influence the development of colitis associated colorectal cancer (CAC). For this study, the goal was to determine the association between colon inflammation, diet and microbiome in the development of CAC in mice. The primary objective of this study was to determine the contribution of gut microbiota from mice donors who have previously consumed one of two basal diets: 1) the standard AIN93G diet, which is designed to promote rodent health; and 2) the total Western diet (TWD), which promotes inflammation- associated colorectal tumorigenesis. The donors’ microbiota was transferred to a cohort of mice who were fed either the AIN93G or the TWD observing the impact of FMT on inflammation and tumorigenesis. Using a 2x2 factorial design, C57BL/6J male mice were fed the standard AIN93G diet or the TWD for 16 weeks while receiving fecal microbiota transfer (FMT) from the mice fed either the AIN93G diet or the TWD from tumor bearing mice in a prior experiment. The azoxymethane + dextran sodium sulfate model of inflammation-associated colorectal cancer was employed to assess the dynamic response of the gut microbiome to basal diet and FMT treatment prior to, during, and after active colitis and at the study end. Prior to fecal transfer, the resident gut microbiome was depleted using an established antibiotic/antifungal oral dosing regimen. Endpoints assessed include colitis, tumorigenesis and histopathological scoring of inflammatory infiltration and tissue damage. Preliminary data analyses show that direct exposure to the TWD in this second study increased colitis symptoms and tumor development, as anticipated based on prior work. However, FMT from mice fed the TWD in the prior study did not increase symptoms of colitis or alter patterns of tumorigenesis in mice fed the standard AIN diet in this second study. These observations suggest that the altered gut microbiome caused by consumption of TWD is likely not the primary factor driving tumorigenesis in this model of CAC. Presentation Time: Wednesday, 12-1 p.m.
Location
Logan, UT
Start Date
4-11-2021 12:00 AM
Included in
Fecal Microbiota Transfer (FMT) From Tumor-Bearing Mice Fed the Total Western Diet (TWD) Does Not Contribute to a Higher Tumor Burden in Mice Fed a Healthy Diet
Logan, UT
Colorectal cancer (CRC) is the third most common cause of cancer death in the United States. Diet and gut microbiome have shown to influence the development of colitis associated colorectal cancer (CAC). For this study, the goal was to determine the association between colon inflammation, diet and microbiome in the development of CAC in mice. The primary objective of this study was to determine the contribution of gut microbiota from mice donors who have previously consumed one of two basal diets: 1) the standard AIN93G diet, which is designed to promote rodent health; and 2) the total Western diet (TWD), which promotes inflammation- associated colorectal tumorigenesis. The donors’ microbiota was transferred to a cohort of mice who were fed either the AIN93G or the TWD observing the impact of FMT on inflammation and tumorigenesis. Using a 2x2 factorial design, C57BL/6J male mice were fed the standard AIN93G diet or the TWD for 16 weeks while receiving fecal microbiota transfer (FMT) from the mice fed either the AIN93G diet or the TWD from tumor bearing mice in a prior experiment. The azoxymethane + dextran sodium sulfate model of inflammation-associated colorectal cancer was employed to assess the dynamic response of the gut microbiome to basal diet and FMT treatment prior to, during, and after active colitis and at the study end. Prior to fecal transfer, the resident gut microbiome was depleted using an established antibiotic/antifungal oral dosing regimen. Endpoints assessed include colitis, tumorigenesis and histopathological scoring of inflammatory infiltration and tissue damage. Preliminary data analyses show that direct exposure to the TWD in this second study increased colitis symptoms and tumor development, as anticipated based on prior work. However, FMT from mice fed the TWD in the prior study did not increase symptoms of colitis or alter patterns of tumorigenesis in mice fed the standard AIN diet in this second study. These observations suggest that the altered gut microbiome caused by consumption of TWD is likely not the primary factor driving tumorigenesis in this model of CAC. Presentation Time: Wednesday, 12-1 p.m.