epiglucan and Colitis

Food polysaccharide 1,3-β-d-glucan (OBG) has been shown to alleviate ulcerative colitis (UC) in a mouse model, but the underlying mechanisms remain unclear. Here, we aimed to investigate potential mechanisms involving interactions among gut microbiota, microbial metabolites and host metabolic function.. OBG alleviated colonic inflammation, barrier dysfunction and intestinal concentrations of short-chain fatty acids in mice with UC. In addition, the relative abundance of Muribaculaceae, Alistipes, Erysipelatoclostridium and Blautia increased, whereas the abundance of Proteus, Lachnospiraceae and Ruminococcus decreased within the gut microbiota upon OBG treatment. Kyoto Encyclopedia of Genes and Genomes analyses showed that intestinal enzymes altered upon OBG treatment were mainly enriched in sub-pathways of amino acid biosynthesis. Metabolomics analyses showed that l-tryptophan, l-tyrosine, l-phenylalanine and l-alanine increased, which is consistent with the predictive metabolism of gut microbiota. Correlation analysis and interaction networks highlighted gut microbiota (especially Lactobacillus, Parabacteroides, Proteus and Blautia), metabolites (especially l-phenylalanine, l-tryptophan, l-tyrosine and acetic acid) and metabolism (phenylalanine, tyrosine and tryptophan biosynthesis) that may be key targets of OBG.. OBG is beneficial to the gut microecological balance in mice with colitis, mainly becaue of its impact on the interactions between gut microbes and amino acids metabolism (especially tyrosine and tryptophan metabolism). © 2022 Society of Chemical Industry.

Topics: Animals; beta-Glucans; Colitis; Colitis, Ulcerative; Colon; Dextran Sulfate; Disease Models, Animal; Gastrointestinal Microbiome; Mice; Mice, Inbred C57BL; Tryptophan

Topics: Animals; beta-Glucans; Colitis; Colitis-Associated Neoplasms; Colonic Neoplasms; Gastrointestinal Microbiome; Mice; Shiitake Mushrooms

Topics: Animals; beta-Glucans; Colitis; Colitis, Ulcerative; Colon; Dextran Sulfate; Dextrans; Disease Models, Animal; Glucans; Inflammation; Interleukin-6; Mesalamine; Mice; Mice, Inbred C57BL; Proto-Oncogene Proteins c-bcl-2

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.. 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.. 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.. 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.

Topics: Animals; beta-Glucans; Colitis; Liver; Mice; Mice, Inbred C57BL; Obesity; Probiotics; RNA, Ribosomal, 16S; Synbiotics

Crohn's disease (CD), a condition characterized by chronic inflammation of the gastrointestinal tract with alternating periods of exacerbation and remission, is becoming common around the world. This study aimed to analyze the molecular mechanisms underlying the anti-inflammatory properties of oat beta-glucans of varying molar masses by modulating the expression of chemokines and their receptors as well as other proteins related to both stages of TNBS (2,4,6-trinitrobenzosulfonic acid)-induced

Topics: Animals; beta-Glucans; Chemokines; Colitis; Colon; Crohn Disease; Inflammation; Rats; Rats, Sprague-Dawley; Receptors, Chemokine

The β-glucan from

Topics: Animals; beta-Glucans; Colitis; Glucans; Mice; Saccharomyces cerevisiae

Topics: Animals; beta-Glucans; Caco-2 Cells; Candida; Colitis; Cytokines; Dextran Sulfate; Disease Models, Animal; Dysbiosis; Humans; Klebsiella pneumoniae; Mice; Mice, Inbred C57BL; Sepsis; Toll-Like Receptor 2

This study focuses on constructing of an anti-inflammatory drug delivery system by encapsulation of berberine in the β-glucan nanoparticles and evaluates its effect on treating ulcerative colitis.. β-Glucan and the anti-inflammatory drug berberine (BER) are self-assembled into nanoparticles to construct a drug delivery system (GLC/BER). The interaction between the drug and the carrier was characterized by circular dichroism, ultraviolet-visible spectroscopy, and dynamic light scattering. The anti-inflammatory effect of the GLC/BER was evaluated through a lipopolysaccharide (LPS)-induced RAW264.7 macrophage inflammation model and a sodium sulfate (DSS)-induced C57BL/6 mouse ulcerative colitis model.. The GLC/BER nanoparticles have a particle size of 80-120 nm and a high encapsulation efficiency of 37.8±4.21%. In the LPS-induced RAW264.7 macrophage inflammation model, GLC/BER significantly promoted the uptake of BER by RAW264.7 cells. RT-PCR and ELISA assay showed that it could significantly inhibit the inflammatory factors including IL-1β, IL-6 and COX-2. Furthermore, GLC/BER shows inhibiting effect on the secretion of pro-inflammatory factors such as IL-1β and IL-6, down-regulating the production of nitrite oxide; in animal studies, GLC/BER was found to exert a relieving effect on mice colitis.. The study found that GLC/BER has an anti-inflammatory effect in vitro and in vivo, and the GLC carrier improves the potency and bioavailability of BER, providing a new type of nanomedicine for the treatment of colitis.

Topics: Animals; Anti-Inflammatory Agents; Berberine; beta-Glucans; Colitis; Colitis, Ulcerative; Inflammation; Interleukin-6; Lipopolysaccharides; Macrophages; Mice; Mice, Inbred C57BL; Nanoparticles

Inflammatory bowel disease (IBD) including Crohn's disease and ulcerative colitis is a chronic intestinal disease most likely associated with gut dysbiosis. Candida related mycobiota has been demonstrated to play a role in IBD progression. Traditional Chinese herbal medicines (TCHMs) with antifungal activity have a potential in prevention and treatment of fungi-related IBD. Sodium houttuyfonate (SH) is a promising anti-Candida TCHMs. In this study, a dextran sulfate sodium induced colitis model with Candida albicans precolonization is established. SH gavage can significantly decrease the fungal burdens in feces and colon tissues, reduce disease activity index score, elongate colon length, and attenuate colonic damages. Moreover, SH markedly inhibits the levels of anti-Saccharomyces cerevisiae antibodies, β-glucan, and proinflammatory cytokine (IL-1β, IL-6, IL-8, TNF-α), and increases anti-inflammatory factor IL-10 level in serum and colon tissue. Further experiments demonstrate that SH could induce β-glucan exposure, priming intestinal macrophages to get rid of colonized C. albicans through the collaboration of Dectin-1 and TLR2/4. With the decreased fungal burden, the protein levels of Dectin-1, TLR2, TLR4, and NF-κBp65 are fallen back, indicating the primed macrophages calm down and the colitis is alleviated. Collectively, these results manifest that SH can attenuate C. albicans associated colitis via β-glucan exposure, deepening our understanding of TCHMs in the prevention and treatment of fungi associated IBD.

Topics: Alkanes; Animals; beta-Glucans; Candida albicans; Colitis; Dextran Sulfate; Dysbiosis; Gastrointestinal Microbiome; Mice; Sulfites

β-glucan consumption is known for its beneficial health effects, but the mode of action is unclear. While humans and mice lack the required enzymes to digest β-glucans, certain intestinal microbes can digest β-glucans, triggering gut microbial changes. Curdlan, a particulate β-glucan isolated from

Topics: Animals; beta-Glucans; Bifidobacterium; Colitis; Colon; Dextran Sulfate; Diet; Gastrointestinal Microbiome; Humans; Mice

Yeast is an integral part of mammalian microbiome, and like commensal bacteria, has the potential of being harnessed to influence immunity in clinical settings. However, functional specificities of yeast-derived immunoregulatory molecules remain elusive. Here we find that while under steady state, β-1,3-glucan-containing polysaccharides potentiate pro-inflammatory properties, a relatively less abundant class of cell surface polysaccharides, dubbed mannan/β-1,6-glucan-containing polysaccharides (MGCP), is capable of exerting potent anti-inflammatory effects to the immune system. MGCP, in contrast to previously identified microbial cell surface polysaccharides, through a Dectin1-Cox2 signaling axis in dendritic cells, facilitates regulatory T (Treg) cell induction from naïve T cells. Furthermore, through a TLR2-dependent mechanism, it restrains Th1 differentiation of effector T cells by suppressing IFN-γ expression. As a result, administration of MGCP display robust suppressive capacity towards experimental inflammatory disease models of colitis and experimental autoimmune encephalomyelitis (EAE) in mice, thereby highlighting its potential therapeutic utility against clinically relevant autoimmune diseases.

Topics: Animals; beta-Glucans; CD4-Positive T-Lymphocytes; Cell Differentiation; Colitis; Cyclooxygenase 2; Dendritic Cells; Encephalomyelitis, Autoimmune, Experimental; Glucans; Homeodomain Proteins; Immunity; Immunomodulation; Lectins, C-Type; Mannans; Mice; Mice, Inbred C57BL; Mice, Knockout; Polysaccharides; Saccharomyces cerevisiae; T-Lymphocytes, Regulatory; Th1 Cells; Zymosan

β-Glucans (BGs), a group of complex dietary polysaccharides (CDPs), are available as dietary supplements. However, the effects of orally administered highly purified BGs on gut inflammation are largely unknown.. The aim of this study was to investigate the impact of orally administering highly purified, yeast-derived BG (YBG; β-1,3/1,6-d-glucan) on susceptibility to colitis.. Eight-week-old C57BL/6 (B6) mice were used in a series of experiments. Experiment (Expt) 1: male and female mice were treated every day, for 40 d, with saline (control) or 250 μg YBG, followed by 2.5% (wt:vol) dextran sulfate sodium (DSS) in drinking water during days 30-35; and colitis severity and intestinal immune phenotype were determined. Expt 2: female B6 mice were treated with saline or YBG for 30 d and intestinal immune phenotype, gut microbiota composition, and fecal SCFA concentrations were determined. Expt 3: female B6 mice were treated as in Expt 2, given drinking water with or without antibiotics [Abx; ampicillin (1 g/L), vancomycin (0.5 g/L), neomycin (1 g/L), and metronidazole (1 g/L)] during days 16-30, and gut immune phenotype and fecal SCFA concentrations were determined. Expt 4: female B6 Foxp3-green fluorescent protein (-GFP) reporter mice were treated as in Expt 3, and intestinal T-regulatory cell (Treg) frequencies and immune phenotypes were determined. Expt 5: female mice were treated as in Expt 1, given drinking water with or without antibiotics during days 16-40, and colitis severity and intestinal cytokine production were determined.. Compared with controls, the YBG group in Expt 1 exhibited suppressive effects on features of colitis, such as loss of body weight (by 47%; P < 0.001), shortening of colon (by 24%; P = 0.016), and histopathology severity score (by 45%; P = 0.01). The YBG group of Expt 2 showed a shift in the abundance of gut microbiota towards Bacteroides (by 16%; P = 0.049) and Verrucomicrobia (mean ± SD: control = 7.8 ± 0.44 vs. YBG = 21.0 ± 9.6%) and a reduction in Firmicutes (by 66%; P < 0.001). The YBG group also showed significantly higher concentrations of fecal SCFAs such as acetic (by 37%; P = 0.016), propionic (by 47%; P = 0.026), and butyric (by 57%; P = 0.013) acids. Compared with controls, the YBG group of Expt 2 showed higher frequencies of Tregs (by 32%; P = 0.043) in the gut mucosa. Depletion of gut microbiota in the YBG group of mice caused diminished fecal SCFA concentrations (Expt 3) and intestinal Treg frequencies (Expt 4). Compared with the YBG group, the YBG-(Abx) group of Expt 5 showed aggravated colitis features including loss of body weight (by >100%; P < 0.01) and colonic inflammation score (by 42%; P = 0.04).. Studies using B6 mice show that dietary BGs are beneficial for promoting intestinal health when the gut microbiota is intact. However, these CDPs may produce adverse effects if gut microbiota is compromised.

Topics: Animals; beta-Glucans; Colitis; Dextran Sulfate; Fatty Acids, Volatile; Feces; Female; Forkhead Transcription Factors; Gastrointestinal Microbiome; Gene Knock-In Techniques; Green Fluorescent Proteins; Immunity; Intestines; Male; Mice; Mice, Inbred C57BL; Polysaccharides; Saccharomyces cerevisiae

Previously, we have shown that oral administration of yeast derived β-1,3/1,6-d-glucan enhances immune regulation and alters the composition of the gut microbiota. However, it is not known if other structurally distinct β-glucans have similar properties. Here, using C57BL/6 mice, we show the potential of a microalgae derived β-1,3-d-glucan, paramylon (PM), in shaping the gut microbiota and modulating the susceptibility to colitis. The community structure within the gut microbiota showed progressive changes including selective enrichment of specific communities and lowered community richness and diversity during prolonged oral treatment with PM. Compared to control mice, the gut microbiota of PM-treated mice had significantly higher abundance of Verrucomicrobia and lower abundance of Firmicutes. Specific taxa that were significantly more abundant in PM-treated mice include

Topics: Animals; Bacteria; beta-Glucans; Colitis; Feces; Female; Gastrointestinal Microbiome; Glucans; Inflammation; Mice; Mice, Inbred C57BL; Microalgae; Prebiotics; Verrucomicrobia

Inflammatory bowel diseases are an important health problem. Therefore, the aim of the present study was to compare the impact of isolated oat beta-glucan fractions of low and high molecular weight, taken as dietary supplementation, on inflammatory markers in the colitis model.. Two groups of Sprague-Dawley rats-control and with experimentally induced colitis-were subsequently divided into three subgroups and fed over 21 days feed supplemented with 1% of low (βGl) or high (βGh) molecular weight oat beta-glucan fraction or feed without supplementation. The level of colon inflammatory markers, cytokines, and their receptors' genes expressions and immune cells numbers were measured by ELISA, RT-PCR, and by flow cytometry methods, respectively.. The results showed moderate inflammation affecting the colon mucosa and submucosa, with significant changes in the number of lymphocytes in the colon tissue, elevated cytokines and eicosanoid levels, as well as disruption of the main cytokine and chemokine cell signaling pathways in colitis rats. Beta-glucans supplementation caused a reverse in the percentage of lymphocytes with stronger effects of βGh and reduction of the levels of the inflammatory markers, and improvement of cytokine and chemokine signaling pathways with stronger effects of βGl supplementation.. The results indicate the therapeutic effect of dietary oat beta-glucan supplementation in the colitis in evident relation to the molecular weight of polymer.

Topics: Animals; Anti-Inflammatory Agents; Avena; beta-Glucans; Colitis; Cytokines; Dietary Supplements; Disease Models, Animal; Gene Expression Regulation; Lymphocyte Count; Male; Molecular Weight; Rats; Rats, Sprague-Dawley; Trinitrobenzenesulfonic Acid

Most of the reported yeast polysaccharides are a mixture of chitin, β-glucan and mannoprotein, leading to different biological activities. Herein, we report the structures and the anti-inflammation of the purified baker's yeast polysaccharides (BBG1-BBG4). Experimental data indicated that BBG1 was a highly branched β-(1,6)-glucan linked to mannoprotein; BBG2 was a linear β-(1,3)-glucan; BBG3 and BBG4 were mixtures of a β-(1,6)-branched β-(1,3)-glucan and a linear β-(1,3)-glucan. Of these, BBG1 exhibited stronger inhibition of pro-inflammatory mediators of NO/iNOS, IL-6, IL-1β, etc. at protein and/or mRNA levels in LPS-stimulated RAW264.7 cells through inhibiting MAPK signalling pathways. Orally administered BBG1 and BBG2 significantly decreased the pro-inflammatory mediators of IL-6, iNOS and IL-1β at protein and/or mRNA levels, as well as colonic mucosal damage and macrophages infiltration in DSS-induced colitis mice. All these findings suggest that yeast polysaccharides have potentials as anti-inflammatory drugs or adjuvants in the intestinal inflammation therapy.

Topics: Administration, Oral; Animals; Anti-Inflammatory Agents; beta-Glucans; Colitis; Cytokines; Dextran Sulfate; Inflammation; Intestinal Mucosa; Male; MAP Kinase Signaling System; Mice; Mice, Inbred C57BL; RAW 264.7 Cells; Saccharomyces cerevisiae

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

Intestinal fungi are increasingly believed to greatly influence gut health. However, the effects of fungi on intestinal inflammation and on gut bacterial constitution are not clear. Here, based on pyrosequencing method, we reveal that fungal compositions vary in different intestinal segments (ileum, cecum, and colon), prefer different colonization locations (mucosa and feces), and are remarkably changed during intestinal inflammation in dextran sulfate sodium (DSS)-colitis mouse models compare to normal controls: Penicillium, Wickerhamomyces, Alternaria, and Candida are increased while Cryptococcus, Phialemonium, Wallemia and an unidentified Saccharomycetales genus are decreased in the guts of DSS-colitis mice. Fungi-depleted mice exhibited aggravated acute DSS-colitis associated with gain of Hallella, Barnesiella, Bacteroides, Alistipes, and Lactobacillus and loss of butyrate-producing Clostridium XIVa, and Anaerostipes compare with normal control. In contrast, bacteria-depleted mice show attenuated acute DSS-colitis. Mice with severely chronic recurrent DSS-colitis show increased plasma (1,3)-β-D-glucan level and fungal translocation into the colonic mucosa, mesenteric lymph nodes and spleen. This work demonstrate the different roles of fungi in acute and chronic recurrent colitis: They are important counterbalance to bacteria in maintaining intestinal micro-ecological homeostasis and health in acutely inflamed intestines, but can harmfully translocate into abnormal sites and could aggravate disease severity in chronic recurrent colitis.

Topics: Acute Disease; Animals; beta-Glucans; Colitis; Colon; Cytokines; Dextran Sulfate; Discriminant Analysis; Disease Models, Animal; Fluconazole; Fungi; Inflammation; Intestinal Mucosa; Least-Squares Analysis; Lymph Nodes; Mice; Mice, Inbred C57BL; Occludin; Proteoglycans; Real-Time Polymerase Chain Reaction; RNA, Ribosomal, 16S; RNA, Ribosomal, 18S; Spleen; Zonula Occludens-1 Protein

β-Glucans have beneficial health effects due to their immune modulatory properties. Oral administration of β-glucans affects tumour growth, microbial infection, sepsis, and wound healing. We hypothesized that pre-treatment with orally delivered soluble and particulate β-glucans could ameliorate the development of aggravate dextran sulfate sodium (DSS) induced intestinal inflammation. To study this, mice were orally pre-treated with β-glucans for 14 days. We tested curdlan (a particulate β-(1,3)-glucan), glucan phosphate (a soluble β-(1,3)-glucan), and zymosan (a particle made from Saccharomyces cerevisiae, which contains around 55% β-glucans). Weight loss, colon weight, and feces score did not differ between β-glucan and vehicle treated groups. However, histology scores indicated that β-glucan-treated mice had increased inflammation at a microscopic level suggesting that β-glucan treatment worsened intestinal inflammation. Furthermore, curdlan and zymosan treatment led to increased colonic levels of inflammatory cytokines and chemokines, compared to vehicle. Glucan phosphate treatment did not significantly affect cytokine and chemokine levels. These data suggest that particulate and soluble β-glucans differentially affect the intestinal immune responses. However, no significant differences in other clinical colitis scores between soluble and particulate β-glucans were found in this study. In summary, β-glucans aggravate the course of dextran sulfate sodium (DSS)-induced intestinal inflammation at the level of the mucosa.

Topics: Administration, Oral; Animals; beta-Glucans; Chemokines; Colitis; Colon; Cytokines; Dextran Sulfate; Glucans; Inflammation; Intestinal Mucosa; Mice, Inbred C57BL; Zymosan

As a water-soluble extracellular β-glucan produced by Agrobacterium sp. ZX09, Salecan has an excellent toxicological profile and exerts multiple physiological effects. The aims of the present study were to investigate the protective effects of a Salecan diet in the well-defined dextran sulphate sodium (DSS) model of experimental murine colitis and to elucidate the mechanism involved in its effects with special attention being paid to its effect on the production of TNF-α, a primary mediator involved in the inflammatory response. Male C57BL/6J mice were fed a diet supplemented with either 4 or 8 % Salecan for 26 d and DSS was administered to induce acute colitis during the last 5 d of the experimental period. Several clinical and inflammatory parameters as well as mRNA expression of TNF-α and Dectin-1 were evaluated. The results indicated that the dietary incorporation of Salecan attenuated the severity of DSS colitis as evidenced by the decreased disease activity index, reduced severity of anaemia, attenuated changes in colon architecture and reduced colonic myeloperoxidase activity. This protection was associated with the down-regulation of TNF-α mRNA levels, which might derive from its ability to increase Dectin-1 mRNA levels. In conclusion, the present study suggests that Salecan contributes to the reduction of colonic damage and inflammation in mice with DSS-induced colitis and holds promise as a new, effective nutritional supplement in the management of inflammatory bowel disease.

Topics: Analysis of Variance; Animals; beta-Glucans; Colitis; Colon; Dextran Sulfate; Dietary Supplements; Disease Models, Animal; Down-Regulation; Inflammation; Intestinal Mucosa; Lectins, C-Type; Male; Mice; Mice, Inbred C57BL; Peroxidase; Real-Time Polymerase Chain Reaction; RNA, Messenger; Tumor Necrosis Factor-alpha

Interleukin-23 (IL-23), a cytokine produced primarily by dendritic cells, is involved in host defense against gut pathogens and promotes innate immunity and inflammatory responses through the IL-23/interleukin-17 axis. We previously reported that extracts from edible mushrooms enhanced antimicrobial α-defensin production n HL60 cells. Because IL-23 is involved in defensin production, we hypothesized that edible mushrooms may modulate its secretion and gut inflammation. Eight-week-old C57BL/6 mice were fed the AIN76 diet or the same diet supplemented with 5% white button (WBM), portabella, or shiitake mushrooms. To assess in vivo and in vitro cytokine secretion, 7 to 8 mice per group received 3% dextran sodium sulfate (DSS) in drinking water during the last 5 days of the 6-week feeding period. To delineate the mechanisms by which mushrooms alter IL-23 secretion, J.744.1 cells were incubated with (100 μg/mL) WBM, portabella, and shiitake extracts without and with 100 μg/mL curdlan (a dectin-1 agonist) or 1 mg/mL laminarin (a dectin-1 antagonist). The dectin-1 receptor is a pattern-recognition receptor found in phagocytes, and its activation promotes antimicrobial innate immunity and inflammatory responses. In DSS-untreated mice, mushrooms significantly increased IL-23 plasma levels but decreased those of interleukin-6 (IL-6) (P < .05). In DSS-treated mice, mushroom-supplemented diets increased IL-6 and IL-23 levels (P < .05). Mushroom extracts potentiated curdlan-induced IL-23 secretion, and mushroom-induced IL-23 secretion was not blocked by laminarin in vitro, suggesting the involvement of both dectin-1-dependent and dectin-1-independent pathways. Although all mushrooms tended to increase IL-6 in the colon, only WBM and shiitake tended to increase IL-23 levels. These data suggest that edible mushrooms may enhance gut immunity through IL-23.

Topics: Animals; Anti-Infective Agents; beta-Glucans; Cell Line; Colitis; Dextran Sulfate; Dietary Supplements; Female; Glucans; Immunity, Innate; Inflammation; Interleukin-17; Interleukin-23; Interleukin-6; Lectins, C-Type; Macrophages; Mice; Mice, Inbred C57BL; Organ Size; Polysaccharides; Regression Analysis; Shiitake Mushrooms; Thymus Gland; Up-Regulation