Vuong Vu1, Karthika Muthuramalingam2, Vineet Singh3, Changlim Hyun4, Young Mee Kim2, Tatsuya Unno5,6, Moonjae Cho7,8,9. 1. Interdisciplinary Graduate Program in Advanced Convergence Technology and Science, Jeju National University, Jeju, 63241, Republic of Korea. 2. Department of Biochemistry, School of Medicine, Jeju National University, Jeju, 63243, Republic of Korea. 3. Faculty of Biotechnology, School of Life Sciences, SARI, Jeju National University, Jeju, 63243, Republic of Korea. 4. Department of Pathology, School of Medicine, Jeju National University, Jeju, 690-756, South Korea. 5. Faculty of Biotechnology, School of Life Sciences, SARI, Jeju National University, Jeju, 63243, Republic of Korea. tatsu@jejunu.ac.kr. 6. Subtropical/Tropical Organism Gene Bank, Jeju National University, Jeju, 63243, Republic of Korea. tatsu@jejunu.ac.kr. 7. Interdisciplinary Graduate Program in Advanced Convergence Technology and Science, Jeju National University, Jeju, 63241, Republic of Korea. moonjcho@jejunu.ac.kr. 8. Department of Biochemistry, School of Medicine, Jeju National University, Jeju, 63243, Republic of Korea. moonjcho@jejunu.ac.kr. 9. Institute of Medical Science, Jeju National University, Jeju, 63241, Republic of Korea. moonjcho@jejunu.ac.kr.
Abstract
PURPOSE: Probiotics and prebiotics are commonly used to improve the gut microbiota. Since prebiotics can support the growth of probiotics, co-administration of these is called synbiotics. It has been demonstrated that obesity-induced gut dysbiosis can worsen inflammatory bowel disease symptoms. This study evaluated how modulation of gut microbiota with Schizophyllum commune-derived β-glucan (BG), probiotics (PRO), and synbiotics containing both BG and PRO (SYN) could improve the symptoms of obesity-associated colitis and hepatic manifestation. METHODS: Mice were fed a normal diet (ND), high-fat diet (HFD), and HFD with different additives (BG, PRO, and SYN) for 12 weeks, followed by 5 days of colitis induction. Mice were sacrificed before and after colitis induction. During the experiment, body weight, food and water consumption, and rectal bleeding were monitored. Proteins from the colon were subjected to western blotting, and serum biomarkers such as alanine transaminase, alkaline phosphatase, triglycerides, and total cholesterol were analyzed. Colon and liver samples were sectioned for histological analysis. The fecal microbiota was analyzed based on partial 16S rRNA gene sequences. RESULTS: Although BG and PRO secured intestinal tight junctions, these two treatments did not modulate inflammatory cell infiltration and inflammatory markers (i.e., IL-6 and TNF-α). In contrast, SYN demonstrated stronger and broader effects in reducing colonic inflammation. While BG treatment increased the abundance of indigenous Lactobacillus, PRO treatment decreased bacterial diversity by suppressing the growth of several species of bacteria. SYN treatment groups, however, supported the growth of both indigenous and supplemented bacteria while maintaining bacterial diversity. CONCLUSION: Obesity-associated colitis can be improved by modulating gut bacteria with β-glucan and probiotics. The co-administration of both outperformed β-glucan and probiotic treatment alone by fostering both indigenous and supplemented probiotic strains.
PURPOSE: Probiotics and prebiotics are commonly used to improve the gut microbiota. Since prebiotics can support the growth of probiotics, co-administration of these is called synbiotics. It has been demonstrated that obesity-induced gut dysbiosis can worsen inflammatory bowel disease symptoms. This study evaluated how modulation of gut microbiota with Schizophyllum commune-derived β-glucan (BG), probiotics (PRO), and synbiotics containing both BG and PRO (SYN) could improve the symptoms of obesity-associated colitis and hepatic manifestation. METHODS: Mice were fed a normal diet (ND), high-fat diet (HFD), and HFD with different additives (BG, PRO, and SYN) for 12 weeks, followed by 5 days of colitis induction. Mice were sacrificed before and after colitis induction. During the experiment, body weight, food and water consumption, and rectal bleeding were monitored. Proteins from the colon were subjected to western blotting, and serum biomarkers such as alanine transaminase, alkaline phosphatase, triglycerides, and total cholesterol were analyzed. Colon and liver samples were sectioned for histological analysis. The fecal microbiota was analyzed based on partial 16S rRNA gene sequences. RESULTS: Although BG and PRO secured intestinal tight junctions, these two treatments did not modulate inflammatory cell infiltration and inflammatory markers (i.e., IL-6 and TNF-α). In contrast, SYN demonstrated stronger and broader effects in reducing colonic inflammation. While BG treatment increased the abundance of indigenous Lactobacillus, PRO treatment decreased bacterial diversity by suppressing the growth of several species of bacteria. SYN treatment groups, however, supported the growth of both indigenous and supplemented bacteria while maintaining bacterial diversity. CONCLUSION: Obesity-associated colitis can be improved by modulating gut bacteria with β-glucan and probiotics. The co-administration of both outperformed β-glucan and probiotic treatment alone by fostering both indigenous and supplemented probiotic strains.