cholecalciferol has been researched along with Colitis* in 13 studies
1 review(s) available for cholecalciferol and Colitis
1 trial(s) available for cholecalciferol and Colitis
12 other study(ies) available for cholecalciferol and Colitis
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Vitamin D3 and Lactobacillus rhamnosus GG/p40 Synergize to Protect Mice From Colitis by Promoting Vitamin D Receptor Expression and Epithelial Proliferation.
While vitamin D (VitD) levels are negatively correlated with inflammatory bowel disease (IBD) activity, VitD supplementation does not reduce IBD severity. The probiotic Lactobacillus rhamnosus GG (LGG), which secretes p40, can upregulate colonic VitD receptor (VDR) expression. We therefore evaluated synergy between VitD3 and LGG/p40 in the treatment of mouse colitis.. A dextran sulfate sodium (DSS) colitis model was established in Vdr+/+ and Vdr-/- mice, and mice were treated with VitD3, LGG, or p40 alone or in combination for 7 to 14 days. Colitis severity was assessed by weight loss, disease activity index (DAI), colon length, histology, and inflammatory cytokine expression together with VDR expression, proliferation, and apoptosis. In vitro, VDR expression and cell viability were assessed in HCT116 cells after stimulation with p40.. Total and nuclear VDR protein expression were lower in DSS-treated Vdr+/+ mice compared with control mice (P < .05). Compared with the DSS group, VitD3 + LGG alleviated colitis as assessed by significantly improved DAI and histological scores, increased colon length, decreased colonic Tnf, and increased Il10 expression together with increased colonic VDR gene and protein expression and increased Ki-67 proliferation index (P < .05). In Vdr-/- mice, VitD3 + LGG had no effect on DSS colitis. In Vdr+/+ mice, VitD3 + p40 also reduced colitis severity according to clinicopathological and immunological metrics and increased VDR expression and epithelial proliferation (P < .05). In HCT116 cells, p40 stimulation increased VDR protein expression and viability (P < .05).. VitD3 and LGG/p40 synergistically improve the severity of colitis by increasing colonic VDR expression and promoting colonic epithelial proliferation.. There is increasing evidence that vitamin D and its associated pathways may be a helpful adjunct to inflammatory bowel disease therapies. This experimental study shows that vitamin D may synergize with the probiotic Lactobacillus rhamnosus GG for enhanced therapeutic effect. Topics: Animals; Cell Proliferation; Cholecalciferol; Colitis; Colon; Dextran Sulfate; Disease Models, Animal; Inflammatory Bowel Diseases; Lacticaseibacillus rhamnosus; Mice; Mice, Inbred C57BL; Receptors, Calcitriol | 2023 |
CCL20 mediates the anti-tumor effect of vitamin D3 in p38MAPK/NF-κB signaling in colitis-associated carcinogenesis.
Vitamin D3 is beneficial in ameliorating or preventing inflammation and carcinogenesis. CCL20 is a potential therapeutic target in carcinogenesis, which mediates the protective effect of vitamin D or vitamin D analogue in autoimmune and cancer diseases. Here we aim to evaluate whether vitamin D3 plays a protective role in colitis-associated colorectal cancer (CAC) by affecting CCL20 and the molecular mechanism. Administration of azoxymethane (AOM) followed with dextran sulfate sodium (DSS) was used to simulate CAC in mouse. After 5-day DSS treatment, vitamin D3 supplementation was for 9 weeks at 60 IU/g/w. We found that dietary vitamin D3 significantly reduced the tumor number and tumor burden in mouse. In-vivo and -vitro, vitamin D3 reduced the levels of CCL20, phospho-p38 MAPK (p-p38) and phospho-NF-κB p65 (p-p65), and the transcriptional activity of NF-κB. Further studies showed that CCL20 mediated the inhibition of vitamin D3 in p38MAPK-mediated NF-κB signaling in vitro. Taken together, vitamin D3 effectively suppressed colonic carcinogenesis in AOM-DSS mouse model. Downregulation of CCL20 may contribute to the preventive effect of vitamin D3 on NF-κB activity. It may merit further clinical investigation as a therapeutic agent against CAC in humans. Topics: Animals; Antineoplastic Agents; Carcinogenesis; Chemokine CCL20; Cholecalciferol; Colitis; Colorectal Neoplasms; Disease Models, Animal; Male; Mice; Mice, Inbred C57BL; NF-kappa B; p38 Mitogen-Activated Protein Kinases; Signal Transduction | 2021 |
Active vitamin D3 attenuates the severity of Salmonella colitis in mice by orchestrating innate immunity.
Salmonella spp. pose major public health problems worldwide. A better understanding of the pathogenesis of these foodborne pathogens is a prerequisite for the design of improved intervention strategies that could reduce the use of antimicrobial agents and drug-resistant Salmonellosis. Accumulating evidence indicates that vitamin D is involved in regulating innate immunity, and may, therefore, play a key role in human responses to infection. Studies have suggested 1,25-dihydroxyvitamin D3 (1,25D3), the active form of vitamin D, effectively ameliorates colitis. These findings have broad implications for the use of vitamin D compounds in colitis. This study investigated the effect of active vitamin D3 on the severity of Salmonella colitis.. A Salmonella colitis model was established with 6-8-week-old male C57BL/6 mice: Streptomycin-pretreated C57BL/6 mice were infected orally with Salmonella enterica serova Typhimurium wild-type strain SL1344 for 48 h. The mice were randomly assigned to control, model, and 1,25(OH). We observed that 1,25D3 reduced the severity of Salmonella colitis in C57BL/6 mice by reducing cecal mIL-1beta, mIL-6, mTNF-alpha, and mIL-8 mRNA expressions, bacterial colonization (CFU/mg tissue) in the liver and spleen, but increased the human β-defensin-2 mRNA and autophagy protein expression, compared to those of the SL1344 infection only.. Our results document that active vitamin D3 reduced Salmonella colitis by decreasing inflammation, and bacterial translocation via induction of killing and autophagic clearance of pathogenic organisms. Topics: Animals; Cholecalciferol; Colitis; Immunity, Innate; Male; Mice; Mice, Inbred C57BL; Salmonella typhimurium | 2021 |
Free versus total serum 25-hydroxyvitamin D in a murine model of colitis.
Inflammatory bowel diseases (IBD) such as ulcerative colitis and Crohn's disease have been linked to vitamin D-deficiency. Using a dextran sodium sulphate (DSS)-induced model of IBD we have shown previously that mice raised on vitamin D-deficient diets from weaning have lower serum 25-hydroxyvitamin D (25OHD) levels and develop more severe colitis compared to vitamin D-sufficient counterparts. We have also shown in vitro that immune responses to 25OHD may depend on 'free' rather than total serum concentrations of 25OHD. To investigate the possible effects of free versus total 25OHD on anti-inflammatory immune responses in vivo we have studied DSS-induced colitis in wild type C57BL/6 mice raised from weaning on diets containing vitamin D2 (D2) or vitamin D3 (D3) only (both 1000 IU/kg feed). 25OHD2 has lower binding affinity for the vitamin D binding protein than 25OHD3 which results in higher levels of free 25OHD2 relative to free 25OHD3 in mice raised on a D2-only diet. Total serum 25OHD concentrations, measured by liquid chromatography-tandem mass spectrometry (LC-MS/MS), showed that D2 mice had significantly lower levels of 25OHD than D3 mice (6.85 ± 2.61 nmol/L vs. 49.16 ± 13.8 nmol/L for D2 and D3 respectively). Despite this, direct ELISA measurement showed no difference in free serum 25OHD levels between D2 and D3 mice (13.62 ± 2.26 pmol/L vs. 14.11 ± 2.24 pmol/L for D2 and D3 respectively). Analysis of DSS-induced colitis also showed no difference in weight loss or disease progression between D2 and D3 mice. These data indicate that despite D2-fed mice being vitamin D-deficient based on serum total 25OHD concentrations, these mice showed no evidence of increased inflammatory colitis disease relative to vitamin D-sufficient D3 mice. We therefore propose that free, rather than total serum 25OHD, may be a better marker of immune responses to vitamin D in vivo. Topics: 25-Hydroxyvitamin D 2; Animals; Calcifediol; Cholecalciferol; Colitis; Ergocalciferols; Male; Mice, Inbred C57BL; Vitamin D; Vitamin D Deficiency; Vitamins | 2019 |
Ultraviolet Irradiation of Skin Alters the Faecal Microbiome Independently of Vitamin D in Mice.
Reduced sunlight exposure has been associated with an increased incidence of Crohn's disease and ulcerative colitis. The effect of ultraviolet radiation (UVR) on the faecal microbiome and susceptibility to colitis has not been explored. C57Bl/6 female mice were fed three different vitamin D-containing diets for 24 days before half of the mice in each group were UV-irradiated (1 kJ/m²) for each of four days, followed by twice-weekly irradiation of shaved dorsal skin for 35 days. Faecal DNA was extracted and high-throughput sequencing of the 16S RNA gene performed. UV irradiation of skin was associated with a significant change in the beta-diversity of faeces compared to nonirradiated mice, independently of vitamin D. Specifically, members of phylum Firmicutes, including Topics: Animal Feed; Animals; Bacteria; Cholecalciferol; Colitis; Cytokines; Dextran Sulfate; Disease Models, Animal; Feces; Female; Gastrointestinal Microbiome; Inflammation Mediators; Mice, Inbred C57BL; Skin; Ultraviolet Rays | 2018 |
E-cadherin Mediates the Preventive Effect of Vitamin D3 in Colitis-associated Carcinogenesis.
Vitamin D3 is beneficial in ameliorating or preventing inflammation and carcinogenesis. Here, we evaluated if vitamin D3 has a preventive effect on colitis-associated carcinogenesis. Administration of azoxymethane (AOM), followed with dextran sulfate sodium (DSS), was used to simulate colitis-associated colon cancer in mice. The supplement of vitamin D3 at different dosages (15, 30, 60 IU·g·w), started before AOM or immediately after DSS treatment (post 60), was sustained to the end of the experiment. Dietary vitamin D3 significantly reduced the number of tumors and tumor burden in a dose-dependent manner. Of note, vitamin D3 in high doses showed significant preventive effects on carcinogenesis regardless of administration before or after AOM-DSS treatment. Cell proliferation decreased in vitamin D3 groups compared with the control group after inhibition of expression of β-catenin and its downstream target gene cyclin D1 in the colon. In vitro, vitamin D3 reduced the transcriptional activity and nuclear level of β-catenin, and it also increased E-cadherin expression and its binding affinity for β-catenin. Moreover, repression of E-cadherin was rescued by supplemental vitamin D3 in mouse colons. Taken together, our results indicate that vitamin D3 effectively suppressed colonic carcinogenesis in the AOM-DSS mouse model. Our findings further suggest that upregulation of E-cadherin contributes to the preventive effect of vitamin D3 on β-catenin activity. Topics: Animals; Azoxymethane; beta Catenin; Cadherins; Carcinogenesis; Cell Proliferation; Cholecalciferol; Colitis; Colon; Colonic Neoplasms; Dextran Sulfate; Disease Models, Animal; Dose-Response Relationship, Drug; Male; Mice; Mice, Inbred C57BL; Up-Regulation; Vitamins | 2017 |
Cholecalciterol cholesterol emulsion ameliorates experimental colitis via down-regulating the pyroptosis signaling pathway.
The therapeutic effect of 1,25(OH)2 vitamin D3 and its analog (paricalcitol) on experimental colitis in animals has been heavily demonstrated. However, the response to Cholecalciterol Cholesterol Emulsion (CCE), a precursor of 1,25(OH)2 vitamin D3, has not yet been reported. Whether pyroptosis is involved in colitic deterioration also remains unclear. Therefore, we adopted molecular biology and histology approaches to examine mechanisms by which CCE was able to regulate experimental colitis in the animal model induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS). Our data revealed that mice displayed a remarkable reduction in colonic histological scores, colonic inflammation and colonic histological damage. In addition, there was an overall improvement in general status (change in body weight, food and water intake, mental status, activity) and a 30% increase in survival rate due to the downregulation of pyroptosis following treatment with CCE. In conclusion, our data have provided evidence that CCE can attenuate the damage of experimental colitis by suppressing pyroptosis signaling. Topics: Animals; Blotting, Western; Calcitriol; Calcium; Caspase 1; Child; Child, Preschool; Cholecalciferol; Cholesterol; Colitis; Colon; Emulsions; Female; Gene Expression; Humans; Interleukin-18; Interleukin-1beta; Male; Mice, Inbred BALB C; Phosphorus; Pyroptosis; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction; Survival Rate; Trinitrobenzenesulfonic Acid; Vitamin D Deficiency; Vitamins | 2016 |
Dietary vitamin D3 deficiency alters intestinal mucosal defense and increases susceptibility to Citrobacter rodentium-induced colitis.
Vitamin D deficiency affects more that 1 billion people worldwide. Although thought to increase risk of bacterial infections, the importance of vitamin D on host defense against intestinal bacterial pathogens is currently unclear since injection of the active form of vitamin D, 1,25(OH)2D3, increased susceptibility to the enteric bacterial pathogen Citrobacter rodentium by suppressing key immune/inflammatory factors. To further characterize the role of vitamin D during bacteria-induced colitis, we fed weanling mice either vitamin D3-deficient or vitamin D3-sufficient diets for 5 wk and then challenged them with C. rodentium. Vitamin D3-deficient mice lost significantly more body weight, carried higher C. rodentium burdens, and developed worsened histological damage. Vitamin D3-deficient mice also suffered greater bacterial translocation to extra-intestinal tissues, including mesenteric lymph nodes, spleen, and liver. Intestinal tissues of infected vitamin D3-deficient mice displayed increased inflammatory cell infiltrates as well as significantly higher gene transcript levels of inflammatory mediators TNF-α, IL-1β, IL-6, TGF-β, IL-17A, and IL-17F as well as the antimicrobial peptide REG3γ. Notably, these exaggerated inflammatory responses accelerated the loss of commensal microbes and were associated with an impaired ability to detoxify bacterial lipopolysaccharide. Overall, these studies show that dietary-induced vitamin D deficiency exacerbates intestinal inflammatory responses to infection, also impairing host defense. Topics: Animals; Bacterial Load; Bacterial Translocation; Cecum; Cholecalciferol; Citrobacter rodentium; Colitis; Colon; Cytokines; Diet; Disease Models, Animal; Enterobacteriaceae Infections; Feces; Female; Host-Pathogen Interactions; Inflammation Mediators; Intestinal Mucosa; Lipopolysaccharide Receptors; Lipopolysaccharides; Mice, Inbred C57BL; Pancreatitis-Associated Proteins; Phosphorylation; Proteins; Time Factors; Vitamin D Deficiency; Weight Loss | 2015 |
High vitamin D3 diet administered during active colitis negatively affects bone metabolism in an adoptive T cell transfer model.
Decreased bone mineral density (BMD) represents an extraintestinal complication of inflammatory bowel disease (IBD). Vitamin D₃ has been considered a viable adjunctive therapy in IBD. However, vitamin D₃ plays a pleiotropic role in bone modeling and regulates the bone formation-resorption balance, depending on the physiological environment, and supplementation during active IBD may have unintended consequences. We evaluated the effects of vitamin D₃ supplementation during the active phase of disease on colonic inflammation, BMD, and bone metabolism in an adoptive IL-10-/- CD4⁺ T cell transfer model of chronic colitis. High-dose vitamin D₃ supplementation for 12 days during established disease had negligible effects on mucosal inflammation. Plasma vitamin D₃ metabolites correlated with diet, but not disease, status. Colitis significantly reduced BMD. High-dose vitamin D₃ supplementation did not affect cortical bone but led to a further deterioration of trabecular bone morphology. In mice fed a high vitamin D₃ diet, colitis more severely impacted bone formation markers (osteocalcin and bone alkaline phosphatase) and increased bone resorption markers, ratio of receptor activator of NF-κB ligand to osteoprotegrin transcript, plasma osteoprotegrin level, and the osteoclast activation marker tartrate-resistant acid phosphatase (ACp5). Bone vitamin D receptor expression was increased in mice with chronic colitis, especially in the high vitamin D₃ group. Our data suggest that vitamin D₃, at a dose that does not improve inflammation, has no beneficial effects on bone metabolism and density during active colitis or may adversely affect BMD and bone turnover. These observations should be taken into consideration in the planning of further clinical studies with high-dose vitamin D₃ supplementation in patients with active IBD. Topics: Adoptive Transfer; Amphiregulin; Animal Feed; Animals; Bone and Bones; Bone Density; CD4-Positive T-Lymphocytes; Cholecalciferol; Chronic Disease; Colitis; Diet; EGF Family of Proteins; Gene Deletion; Glycoproteins; Intercellular Signaling Peptides and Proteins; Interleukin-10; Mice; Mice, Knockout; Vitamins | 2013 |
The vitamin D analog TX527 ameliorates disease symptoms in a chemically induced model of inflammatory bowel disease.
The vitamin D system plays a critical role in inflammatory bowel disease as evidenced by the finding that both vitamin D deficient mice and vitamin D receptor knockout mice are extremely sensitive to dextran sodium sulfate (DSS)-induced colitis. Moreover, the active form of vitamin D, 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3] is an important immunomodulator that ameliorates the pathogenesis of inflammatory bowel disease. However, therapeutic application of 1,25(OH)2D3 is hampered by its calcemic activity. Previous work illustrated that the analog 1α,25(OH)2-19-nor-14,20-bisepi-23-yne-vitamin D3 (TX527) has potent antiproliferative effects with limited calcemic activity. In the present study we demonstrated that TX527 ameliorated disease symptoms in a DSS-induced model of inflammatory bowel disease. TX527 significantly attenuated disease scores, by suppressing bleeding and diarrhea. Colon length was significantly elevated at the end of the experiment. Histological examination indicated that TX527 diminished mucosal damage and crypt loss and suppressed the infiltration of immune cells in DSS-induced colitis mice. Furthermore, transcript levels of inflammatory cytokines such as IL-1, IL-6, IFN-γ and TNF-α were significantly down-regulated in colonic mucosa of mice with colitis. Moreover, transcript levels of the gastrointestinal glutathione peroxidase 2, which acts as a radical scavenger, were significantly down-regulated after TX527 treatment in DSS-colitis mice. These results indicate that TX527 may have a therapeutic value in the setting of inflammatory bowel disease. This article is part of a Special Issue entitled 'Vitamin D Workshop'. Topics: Alkynes; Animals; Calcium; Cholecalciferol; Colitis; Cytokines; Dextran Sulfate; Disease Models, Animal; Down-Regulation; Female; Glutathione Peroxidase; Inflammatory Bowel Diseases; Mice; Mice, Inbred C57BL; Oxidative Stress | 2013 |
A vitamin D analogue inhibits colonic carcinogenesis in the AOM/DSS model.
The azoxymethane (AOM) model recapitulates many features of human colon cancer, lacking an inflammatory component. Dextran sulfate sodium (DSS) induces colitis and promotes AOM-induced colon cancer in mice. Vitamin D analogues are anti-inflammatory and chemopreventive in models of colon cancer. Our aim was to evaluate the anti-inflammatory and chemopreventive efficacy of the vitamin D analogue Ro26-2198 in the AOM/DSS model and in vitro in HCA-7 colon cancer cells.. A/J mice received Ro26-2198 (0.01 microg/kg body wt/day x 28 days) or vehicle by mini-osmotic pump. Animals were treated with a single dose of AOM (5 mg/kg body wt) or vehicle 1 week after pump insertion. Mice received 3% DSS or water x 7 days beginning week 3. Animals were sacrificed after 8 weeks and colon segments were fixed in formalin or flash-frozen. Hematoxylin and eosin colonic sections were examined for dysplasia and colonic lysates were assessed for c-Myc, cyclooxygenase 2, and phospho-(active) extracellular signal regulated kinase (ERK) by Western blotting. For in vitro studies, HCA-7 cells were treated with Ro26-2198 followed by interleukin-1beta (IL-1beta). Proliferation was measured by WST-1 assay.. Ro26-2198 delayed the onset of clinical colitis. Several dysplastic foci were present in the AOM/DSS group; none were found in the Ro26-2198 group. Compared with control, AOM/DSS significantly increased c-Myc (15-fold), cyclooxygenase 2 (COX-2) (2.5-fold), and pERK (10-fold), and Ro26-2198 abolished these increases. In vitro, Ro26-2198 inhibited IL-1beta-induced ERK activation and COX-2 induction and decreased HCA-7 cell proliferation.. Ro26-2198 inhibited proliferative (ERK, c-Myc) and pro-inflammatory (COX-2) signals and progression to dysplasia, suggesting chemopreventive efficacy in this model of colitis-associated carcinogenesis. Topics: Adenocarcinoma; Animals; Anti-Inflammatory Agents; Cell Division; Cell Line, Tumor; Cholecalciferol; Colitis; Colon; Colonic Neoplasms; Cyclooxygenase 2; Disease Models, Animal; Extracellular Signal-Regulated MAP Kinases; Humans; Interleukin-1beta; Male; MAP Kinase Signaling System; Mice; Mice, Inbred A; Proto-Oncogene Proteins c-myc; Up-Regulation | 2007 |
Control of the innate epithelial antimicrobial response is cell-type specific and dependent on relevant microenvironmental stimuli.
Immune defence against microbes depends in part on the production of antimicrobial peptides, a process that occurs in a variety of cell types but is incompletely understood. In this study, the mechanisms responsible for the induction of cathelicidin and beta-defensin antimicrobial peptides were found to be independent and specific to the cell type and stimulus. Vitamin D3 induced cathelicidin expression in keratinocytes and monocytes but not in colonic epithelial cells. Conversely, butyrate induced cathelicidin in colonic epithelia but not in keratinocytes or monocytes. Distinct factors induced beta-defensin expression. In all cell types, vitamin D3 activated the cathelicidin promoter and was dependent on a functional vitamin D responsive element. However, in colonic epithelia butyrate induced cathelicidin expression without increasing promoter activity and vitamin D3 activated the cathelicidin promoter without a subsequent increase in transcript accumulation. Induction of cathelicidin transcript correlated with increased processed mature peptide and enhanced antimicrobial activity against Staphylococcus aureus. However, induction of beta-defensin-2 expression did not alter the innate antimicrobial capacity of cells in culture. These data suggest that antimicrobial peptide expression is regulated in a tissue-specific manner at transcriptional, post-transcriptional and post-translational levels. Furthermore, these data show for the first time that innate antimicrobial activity can be triggered independently of the release of other pro-inflammatory molecules, and suggest strategies for augmenting innate immune defence without increasing inflammation. Topics: Antimicrobial Cationic Peptides; Bacterial Infections; beta-Defensins; Blotting, Western; Butyrates; Cathelicidins; Cells, Cultured; Cholecalciferol; Colitis; Epithelial Cells; Gene Expression Regulation; Humans; Immunity, Innate; Immunohistochemistry; Keratinocytes; Monocytes; Mutagenesis, Site-Directed; Promoter Regions, Genetic; Reverse Transcriptase Polymerase Chain Reaction; Skin Diseases, Bacterial; Transfection | 2006 |