epiglucan and Inflammatory-Bowel-Diseases

β-Glucan, an essential natural polysaccharide widely distributed in cereals and microorganisms, exhibits extensive biological activities, including immunoregulation, anti-inflammatory, antioxidant, antitumor properties, and flora regulation. Recently, increasing evidence has shown that β-glucan has activities that may be useful for treating intestinal diseases, such as inflammatory bowel disease (IBD), and colorectal cancer. The advantages of β-glucan, which include its multiple roles, safety, abundant sources, good encapsulation capacity, economic development costs, and clinical evidence, indicate that β-glucan is a promising polysaccharide that could be developed as a health product or medicine for the treatment of intestinal disease. Unfortunately, few reports have summarized the progress of studies investigating natural β-glucan in intestinal diseases. This review comprehensively summarizes the structure-activity relationship of β-glucan, its pharmacological mechanism in IBD and colorectal cancer, its absorption and transportation mechanisms, and its application in food, medicine, and drug delivery, which will be beneficial to further understand the role of β-glucan in intestinal diseases.

Topics: Anti-Inflammatory Agents; Antioxidants; beta-Glucans; Colorectal Neoplasms; Dietary Carbohydrates; Humans; Inflammatory Bowel Diseases; Polysaccharides

Progress in genomic analysis has resulted in the proposal that the intestinal microbiota is a crucial environmental factor in the development of multifactorial diseases, such as obesity, diabetes, rheumatoid arthritis, and inflammatory bowel diseases represented by Crohn's disease and ulcerative colitis. Dysregulated gut microbiome contributes to the pathogenesis of such disorders; however, there are few effective treatments for controlling only disease-mediating bacteria. Here, we review current knowledge about the intestinal microbiome in health and disease, and discuss a regulatory strategy using a parenteral vaccine with emulsified curdlan and CpG oligodeoxynucleotides, which we have recently developed. Unlike other conventional injectable immunizations, our vaccine contributes to the induction of antigen-specific systemic and mucosal immunity. This vaccine strategy can prevent infectious diseases such as

Topics: Administration, Mucosal; Arthritis, Rheumatoid; Bacterial Vaccines; beta-Glucans; Diabetes Mellitus, Type 2; Dysbiosis; Gastrointestinal Microbiome; Humans; Immunity, Mucosal; Immunization Schedule; Immunization, Secondary; Immunoglobulin A; Inflammatory Bowel Diseases; Injections, Intramuscular; Intestinal Mucosa; Obesity; Oligodeoxyribonucleotides; Polysaccharides, Bacterial; Vaccines, Synthetic

To evaluate the efficacy of a mixture of beta-glucan, inositol and digestive enzymes in improving gastrointestinal symptoms in patients affected by inflammatory bowel disease (IBD)-irritable bowel syndrome (IBS).. The study was conducted at the IBD Unit of the University of Catanzaro. Forty-three IBD patients with IBS symptoms were included in the study. IBD diagnosis was performed by clinical, endoscopic, histological and radiological criteria. Patients were in clinical remission and in treatment only with systemical and topical mesalamine. All study participants fulfilled the Rome III criteria for the diagnosis of IBS. The study participants were randomized into 2 groups: group A (n=23) received conventional treatment (systemical and topical mesalamine) plus a mixture of beta-glucan, inositol and digestive enzymes (one tablet after lunch and dinner) for four consecutive weeks; group B (n=20) received only conventional treatment. The prevalence and intensity of gastrointestinal (GI) symptoms were evaluated both at the enrollment (T0) and after four weeks of treatment (T1).. Patients who received mesalamine plus the mixture of beta-glucan, inositol and digestive enzymes (group A) reported a reduction in abdominal pain together with reduction in bloating and flatulence after four weeks of treatment. Importantly, an overall improvement in the general well-being has been recorded. Patients who underwent only mesalamine treatment (group B) reported a mild reduction in the evacuative urgency without any other improvements.. We have shown that supplementation with a mixture of beta-glucan, inositol and digestive enzymes reduces bloating, flatulence and abdominal pain, improving the overall clinical condition of IBD-IBS patients.

Topics: Abdominal Pain; Anti-Inflammatory Agents, Non-Steroidal; beta-Glucans; Biological Factors; Drug Combinations; Drug Therapy, Combination; Enzyme Therapy; Female; Flatulence; Gastrointestinal Agents; Humans; Inflammatory Bowel Diseases; Inositol; Irritable Bowel Syndrome; Male; Mesalamine; Middle Aged; Quality of Life

We have recently demonstrated that we could enhance glucan content in Pleurotus eryngii following cultivation of the mushrooms on a substrate containing different concentrations of olive mill solid waste (OMSW). These changes are directly related to the content of OMSW in the growing substrate. Using dextran sulfate sodium (DSS)-in-flammatory bowel disease (IBD) mice model, we measured the colonic inflammatory response to the different glucan preparations. We found that the histology damaging score (HDS) resulting from DSS treatment reach a value of 11.8 ± 2.3 were efficiently downregulated by treatment with the fungal extracted glucans. Glucans extracted from stalks cultivated at 20% OMSW downregulated to a HDS value of 6.4 ± 0.5 whereas those cultivated at 80% OMSW showed the strongest effects (5.5 ± 0.6). Similar downregulatory effects were obtained for expression of various intestinal cytokines. All tested glucans were equally effective in regulating the number of CD14/CD16 monocytes from 18.2 ± 2.7% for DSS to 6.4 ± 2.0 for DSS + glucans extracted from stalks cultivated at 50% OMSW. We tested the effect of glucans on lipopolysaccharide-induced production of TNF-α, which demonstrated that stalk-derived glucans were more effective than caps-derived glucans. Isolated glucans competed with anti-Dectin-1 and anti-CR3 antibodies, indicating that they contain β-glucans recognized by these receptors. In conclusion, the most effective glucans in ameliorating IBD-associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii grown at higher concentrations of OMSW. We conclude that these stress-induced growing conditions may be helpful in selecting more effective glucans derived from edible mushrooms.

Topics: Agaricales; beta-Glucans; Cytokines; Gene Expression Regulation; Glucans; Humans; Immunologic Factors; Inflammation; Inflammatory Bowel Diseases; Olea; Pleurotus; Tumor Necrosis Factor-alpha

Inflammatory bowel diseases (IBD) are a multifactorial disorder. Our understanding of the role of bacteria in the pathogenesis of IBD has increased substantially; however, only scarce data exist regarding the role of commensal fungi in maintaining intestinal homeostasis and triggering IBD. Candida albicans (C. albicans) is a member of the intestinal mycobiome and proposed to contribute to IBD pathogenesis. We aimed to investigate the influence of the two morphologies of C. albicans, yeast and hypha, on epithelial cells and T cells from IBD patients versus healthy controls. We found that C. albicans was recognized by both epithelial cells lines and T cells. In the intestinal epithelial cell line, Caco-2, response to hypha was different than to yeast cells, and this was mimicked by synthetic β-glucans and Pam3CSK4. Unstimulated T cells exhibited increased activation and pro-inflammatory cytokine secretion upon exposure, while there was no effect on apoptosis or proliferation. In contrast, C. albicans-challenged CD3-stimulated T-cells exhibited decreased activation, cytokine secretion, apoptosis, and proliferation, suggesting reciprocal responsiveness to C. albicans. Glycans alone did not mimic abovementioned influences on T cells, suggesting alternative modes of recognition. In conclusion, we provide evidence for glycan dependent and independent recognition of C. albicans by epithelial cells and T cells.

Topics: Apoptosis; beta-Glucans; Caco-2 Cells; Candida albicans; Candidiasis; Cell Line; Cell Line, Tumor; Cell Proliferation; Epithelial Cells; Host-Pathogen Interactions; Humans; Hyphae; Inflammatory Bowel Diseases; Intestinal Mucosa; Intestines; T-Lymphocytes

Mushrooms have been previously investigated for their immune-modulating and anti-inflammatory properties. We examined whether the anti-inflammatory properties of Sarcodon aspratus ethanol extract (SAE) could elicit protective effects against dextran sulfate sodium (DSS)-induced colitis in vivo. Male C57/BL6 mice were randomly assigned to 1 of 4 treatment groups: control (CON; n = 8), DSS-treated (DSS; n = 9), DSS+SAE at 50 mg/kg BW (SAE50; n = 8), and DSS+SAE at 200 mg/kg BW groups (SAE200; n = 9). DSS treatment induced significant weight loss, which was significantly recovered by SAE200. Although SAE did not affect DSS-mediated reductions in colon length, it improved diarrhea and rectal bleeding induced by DSS. SAE at 200 mg/kg BW significantly attenuated IL-6 and enhanced IL-10 expression in mesenteric lymph nodes (MLN), and significantly reduced IL-6 levels in splenocytes. SAE200 also significantly attenuated DSS-induced increase in IL-6 and IL-1β, and reductions in IL-10 in colon tissue. High levels of SAE were also observed to significantly decrease inflammatory COX-2 expression that was upregulated by DSS in mice colon. These findings may have relevance for novel therapeutic strategies to mitigate inflammatory bowel disease-relevant inflammatory responses, via the direct and indirect anti-inflammatory activity of SAE. We also found that SAE harbors significant quantities of total fiber and β-glucan, suggesting a possible role for these components in protection against DSS-mediated colitis.

Topics: Animals; Anti-Inflammatory Agents; Basidiomycota; beta-Glucans; Biological Products; Colitis; Colon; Cyclooxygenase 2; Cytokines; Dextran Sulfate; Dietary Fiber; Inflammation; Inflammatory Bowel Diseases; Interleukin-10; Interleukin-1beta; Interleukin-6; Lymph Nodes; Male; Mesentery; Mice; Mice, Inbred C57BL; Random Allocation

Bacterial β-(1,3)-glucan has more advantages in terms of cost, yield and efficiency than that derived from mushrooms, plants, yeasts and fungi. We have previously developed a novel and high-yield β-(1,3)-glucan produced by Agrobacterium sp. R259. This study aimed to elucidate the functional mechanism and therapeutic efficacy of bacterial β-(1,3)-glucan in dextran sulfate sodium (DSS)-induced inflammatory bowel disease (IBD).Mice were orally pretreated with bacterial β-(1,3)-glucan at daily doses of 2.5 or 5mg/kg for 2 weeks. After 6 days of DSS treatment, clinical assessment of IBD severity and expression of pro-inflammatory cytokines were evaluated. In vivo cell proliferation was examined by immunohistochemistry using Ki-67 and ER-TR7 antibodies. The frequency of regulatory T cells (Tregs) was analyzed by flow cytometry. Natural killer (NK) activity and IgA level were evaluated using NK cytotoxicity assay and ELISA.The deterioration of body weight gain, colonic architecture, disease score and histological score was recovered in DSS-induced IBD mice when pretreated with bacterial β-(1,3)-glucan. The recruitment of macrophages and the gene expression of proinflammatory cytokines, such as IL-1β, IL-6 and IL-17A/F, were markedly decreased in the colon of β-(1,3)-glucan-pretreated mice. β-(1,3)-Glucan induced the recovery of Tregs in terms of their frequency in DSS-induced IBD mice. Intriguingly, β-(1,3)-glucan reversed the functional defects of NK cells and excessive IgA production in DSS-induced IBD mice.We conclude that bacterial β-(1,3)-glucan prevented the progression of DSS-induced IBD by recovering the reduction of Tregs, functional defect of NK cells and excessive IgA production.

Topics: Agrobacterium; Animals; Anti-Inflammatory Agents; beta-Glucans; Cell Proliferation; Colon; Cytokines; Dextran Sulfate; Epithelial Cells; Feces; Fibroblasts; Gene Expression; Immunoglobulin A; Inflammatory Bowel Diseases; Killer Cells, Natural; Lymph Nodes; Male; Mice, Inbred C57BL; Proteoglycans; Reactive Oxygen Species; T-Lymphocytes, Regulatory

β-Glucan is known to have anti-inflammatory properties, and several studies have demonstrated the beneficial effects of dietary β-glucan on inflammatory bowel disease (IBD). However, it is unknown how β-glucan mediates its protective effects on IBD. Therefore, we used a well-established mouse model for IBD, interleukin (IL)-10(-/-) mice, to explore the protective effects of β-glucan on IBD-like symptoms caused by IL-10 deficiency. The mice were divided into two groups: IL-10(-/-) and IL-10(-/-) + β-glucan treatment groups. IL-10(-/-) mice treated with dietary β-glucan exhibited less inflammation within the colon. The levels of immunoglobulins A and E were lower in the serum, spleen, mesenteric lymph nodes, and Peyer's patches in the IL-10(-/-) mice compared with the IL-10(-/-) + β-glucan mice. Also, the expression of pro-inflammatory cytokines was lower in the IL-10(-/-) + β-glucan mice compared with the IL-10(-/-) mice. Histological analysis also revealed that administration of dietary β-glucan in IL-10(-/-) mice reduced colonic tissue damage. Finally, the expression of the pro-inflammatory cytokine tissue necrosis factor-α was significantly lower with dietary β-glucan treatment in IL-10(-/-) mice. In conclusion, dietary β-glucan reduces the inflammation associated with IBD caused by IL-10 deficiency.

Topics: Animals; beta-Glucans; Blotting, Western; Colon; Diet; Disease Models, Animal; Immunoglobulin A; Immunoglobulin E; Inflammation; Inflammatory Bowel Diseases; Interleukin-10; Male; Mice; Mice, Knockout; Peyer's Patches