Inflammatory bowel disease (IBD) is a common ailment affecting people of all ages. Even though the pathogenesis of IBD has not been fully elucidated, there is evidence that it involves interactions between genetic susceptibility, aberrant activation of the immune system, and the environment. Inflammation of the colon (colitis) results in pain, diarrhea, hemorrhage, and weight loss. Within the colon, the family of mucins (MUC) and trefoil factors (TFF) facilitate mucosal protection. Recent studies found that probiotic administration could influence the colonic mucin layer. Additionally, food components may affect gut microflora or have influence on the mucin barrier. Our aims were to explore the role of probiotic administration in modulating MUC and TFF gene expression in the dextran sodium sulfate (DSS) induced colitis mouse model, and to examine interactions with casein, whey, or soy protein diets. C57BL/6 mice were assigned to three diet groups. Diets were formulated to substitute casein, whey or soy protein on an equivalent basis. On day 6, each diet group was divided into 2 groups, with or without Lactobacillus rhamnosus GG (LGG) added daily to the diet. Starting on day 12 the mice were given 2% DSS in drinking water for 4 days and then euthanized 1 day later. A casein diet group with neither LGG nor DSS treatment served as a control. Colon tissues and cecal samples were collected and analyzed by quantitative RT-PCR. LGG-specific gene expression was found in cecum contents of all mice given LGG but none of the untreated mice. Mice fed whey protein had significantly higher LGG quantity compared to mice fed casein diets. Colonic MUC1 and TFF3 gene expression were increased by DSS treatment. In mice fed soy protein, induction of MUC1 and TFF3 expression after DSS was suppressed. Mice fed whey protein had intermediate TFF3 gene expression compared to the other diet groups. There was no overall probiotic effect on any of the parameters. As a marker of inflammation, TNF-α gene expression was increased after DSS treatment. Mice fed soy protein, however, had suppressed TNF-α expression compared to the other treatment groups, which was consistent with the colon length change and colonic inflammation score. In conclusion, soy protein suppressed the DSS-induced inflammatory stimulation of MUC, TFF and TNF-α gene expression independently of the probiotic. Whey protein may act as a prebiotic in the colon to increase microbial survival, but these factors failed to prevent the inflammatory response. Future studies are needed to identify the bioactive components in the soy protein that modulate the barrier function in the colon and have protective effects against colitis.
|Degree||Master of Science, Nutritional Sciences|
|Notes||This thesis was found at the Digital Repository for Iowa State University: http://lib.dr.iastate.edu/|
|University||Iowa State University|