Inflammatory Bowel Diseases (IBD) cause chronic inflammation of the gastrointestinal tract and debilitating symptoms in those suffering from the diseases. After inducing colitis in a mouse model using Dextran Sulfate Sodium (DSS), prebiotics inulin and oligofructose enriched inulin (OEI) were used as treatments to determine their effects on the gut microbial community, physiological healing process, and immune response in the mice after initial inflammation and before subsequent inflammation, or relapse. The treatment with inulin led to an increase in regulatory T cell number, but this increase was not as significant as the increase induced by the OEI. Inulin increased the inflammation in the mouse colon, whereas inflammation was decreased in the colons of the mice treated with OEI. A three percent increase in butyrate producing bacteria, Clostridium cluster XIVa spp., was observed in mice treated with OEI before the relapse period when compared to untreated mice with colitis. The proposed mechanism for how the OEI led to decreased inflammation in the colons of the treated mice was that the introduction of the prebiotic allowed for an increase in butyrate producing Clostridium cluster XIVa spp., which led to a direct increase in butyrate production in the colon. In turn, this butyrate production led to an increase in differentiation of regulatory T cells and an overall reduction of the immune response and inflammation in the mice treated with OEI. This reduction of immune response and inflammation allowed the mice that were treated with OEI to be more resistant to induced relapse.
","abstract_html":"<p>Inflammatory Bowel Diseases (IBD) cause chronic inflammation of the gastrointestinal tract and debilitating symptoms in those suffering from the diseases. After inducing colitis in a mouse model using Dextran Sulfate Sodium (DSS), prebiotics inulin and oligofructose enriched inulin (OEI) were used as treatments to determine their effects on the gut microbial community, physiological healing process, and immune response in the mice after initial inflammation and before subsequent inflammation, or relapse. The treatment with inulin led to an increase in regulatory T cell number, but this increase was not as significant as the increase induced by the OEI. Inulin increased the inflammation in the mouse colon, whereas inflammation was decreased in the colons of the mice treated with OEI. A three percent increase in butyrate producing bacteria, <em>Clostridium cluster XIVa </em>spp., was observed in mice treated with OEI before the relapse period when compared to untreated mice with colitis. The proposed mechanism for how the OEI led to decreased inflammation in the colons of the treated mice was that the introduction of the prebiotic allowed for an increase in butyrate producing <em>Clostridium cluster XIVa </em>spp., which led to a direct increase in butyrate production in the colon. In turn, this butyrate production led to an increase in differentiation of regulatory T cells and an overall reduction of the immune response and inflammation in the mice treated with OEI. This reduction of immune response and inflammation allowed the mice that were treated with OEI to be more resistant to induced relapse.</p>","abstract_has_math":false,"creators":["Davis, Krystyn Elizabeth"],"institution":null,"degree_name":"Master of Science (MS)","degree_level":"Masters Thesis","degree_discipline":"Biological Sciences","degree_department":null,"school":null,"contributors":["Shiao Wang","Fengwei Bai","Hao Xu"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2016,"date_issued":"2016-08-01T07:00:00Z","date_published":"2016-08-01T07:00:00Z","updated_at":"2026-07-24T05:44:34Z","subjects":["Inflammatory Bowel Disease","colitis","prebiotics","gut microbiota","regulatory T cells","gut bacteria","Alternative and Complementary Medicine","Bacteria","Digestive, Oral, and Skin Physiology","Digestive System","Digestive System Diseases","Medical Immunology"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://aquila.usm.edu/masters_theses/194","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Shiao Wang","Fengwei Bai","Hao Xu"]},{"key":"dc:creator","label":"Author","values":["Davis, Krystyn Elizabeth"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2016-06-29T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biological Sciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Masters Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science (MS)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Inflammatory Bowel Disease","colitis","prebiotics","gut microbiota","regulatory T cells","gut bacteria","Alternative and Complementary Medicine","Bacteria","Digestive, Oral, and Skin Physiology","Digestive System","Digestive System Diseases","Medical Immunology"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://aquila.usm.edu/masters_theses/194"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Inflammatory Bowel Diseases (IBD) cause chronic inflammation of the gastrointestinal tract and debilitating symptoms in those suffering from the diseases. After inducing colitis in a mouse model using Dextran Sulfate Sodium (DSS), prebiotics inulin and oligofructose enriched inulin (OEI) were used as treatments to determine their effects on the gut microbial community, physiological healing process, and immune response in the mice after initial inflammation and before subsequent inflammation, or relapse. The treatment with inulin led to an increase in regulatory T cell number, but this increase was not as significant as the increase induced by the OEI. Inulin increased the inflammation in the mouse colon, whereas inflammation was decreased in the colons of the mice treated with OEI. A three percent increase in butyrate producing bacteria, Clostridium cluster XIVa spp., was observed in mice treated with OEI before the relapse period when compared to untreated mice with colitis. The proposed mechanism for how the OEI led to decreased inflammation in the colons of the treated mice was that the introduction of the prebiotic allowed for an increase in butyrate producing Clostridium cluster XIVa spp., which led to a direct increase in butyrate production in the colon. In turn, this butyrate production led to an increase in differentiation of regulatory T cells and an overall reduction of the immune response and inflammation in the mice treated with OEI. This reduction of immune response and inflammation allowed the mice that were treated with OEI to be more resistant to induced relapse.
"]},{"key":"dc:title","label":"Title","values":["Effects of Prebiotics on Gut Bacterial Communities and Healing of Induced Colitis in Mice"]}]}],"canonical_facts":{"dc:contributor":["Shiao Wang","Fengwei Bai","Hao Xu"],"dc:creator":["Davis, Krystyn Elizabeth"],"dc:date.available":["2016-06-29T07:00:00Z"],"dc:description.abstract":["Inflammatory Bowel Diseases (IBD) cause chronic inflammation of the gastrointestinal tract and debilitating symptoms in those suffering from the diseases. After inducing colitis in a mouse model using Dextran Sulfate Sodium (DSS), prebiotics inulin and oligofructose enriched inulin (OEI) were used as treatments to determine their effects on the gut microbial community, physiological healing process, and immune response in the mice after initial inflammation and before subsequent inflammation, or relapse. The treatment with inulin led to an increase in regulatory T cell number, but this increase was not as significant as the increase induced by the OEI. Inulin increased the inflammation in the mouse colon, whereas inflammation was decreased in the colons of the mice treated with OEI. A three percent increase in butyrate producing bacteria, Clostridium cluster XIVa spp., was observed in mice treated with OEI before the relapse period when compared to untreated mice with colitis. The proposed mechanism for how the OEI led to decreased inflammation in the colons of the treated mice was that the introduction of the prebiotic allowed for an increase in butyrate producing Clostridium cluster XIVa spp., which led to a direct increase in butyrate production in the colon. In turn, this butyrate production led to an increase in differentiation of regulatory T cells and an overall reduction of the immune response and inflammation in the mice treated with OEI. This reduction of immune response and inflammation allowed the mice that were treated with OEI to be more resistant to induced relapse.
"],"dc:identifier":["https://aquila.usm.edu/masters_theses/194"],"dc:subject":["Inflammatory Bowel Disease","colitis","prebiotics","gut microbiota","regulatory T cells","gut bacteria","Alternative and Complementary Medicine","Bacteria","Digestive, Oral, and Skin Physiology","Digestive System","Digestive System Diseases","Medical Immunology"],"dc:title":["Effects of Prebiotics on Gut Bacterial Communities and Healing of Induced Colitis in Mice"],"thesis:degree_discipline":["Biological Sciences"],"thesis:degree_level":["Masters Thesis"],"thesis:degree_name":["Master of Science (MS)"]},"updated_at":"2026-07-24T05:44:34Z"}