orabase has been researched along with Colitis* in 8 studies
8 other study(ies) available for orabase and Colitis
Article | Year |
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The Emulsifier Carboxymethylcellulose Induces More Aggressive Colitis in Humanized Mice with Inflammatory Bowel Disease Microbiota Than Polysorbate-80.
Commonly used synthetic dietary emulsifiers, including carboxymethylcellulose (CMC) and polysorbate-80 (P80), promote intestinal inflammation. We compared abilities of CMC vs. P80 to potentiate colitis and impact human microbiota in an inflammatory environment using a novel colitis model of ex-germ-free (GF) IL10 Topics: Animals; Biomarkers; Body Weight; Carboxymethylcellulose Sodium; Colitis; Colon; Emulsifying Agents; Feces; Female; Gastrointestinal Microbiome; Gene Expression Regulation; Humans; Inflammation; Inflammatory Bowel Diseases; Male; Metabolic Networks and Pathways; Mice, Inbred C57BL; Polysorbates; RNA, Messenger | 2021 |
Dietary Emulsifier-Induced Low-Grade Inflammation Promotes Colon Carcinogenesis.
The increased risks conferred by inflammatory bowel disease (IBD) to the development of colorectal cancer gave rise to the term "colitis-associated cancer" and the concept that inflammation promotes colon tumorigenesis. A condition more common than IBD is low-grade inflammation, which correlates with altered gut microbiota composition and metabolic syndrome, both present in many cases of colorectal cancer. Recent findings suggest that low-grade inflammation in the intestine is promoted by consumption of dietary emulsifiers, a ubiquitous component of processed foods, which alter the composition of gut microbiota. Here, we demonstrate in a preclinical model of colitis-induced colorectal cancer that regular consumption of dietary emulsifiers, carboxymethylcellulose or polysorbate-80, exacerbated tumor development. Enhanced tumor development was associated with an altered microbiota metagenome characterized by elevated levels of lipopolysaccharide and flagellin. We found that emulsifier-induced alterations in the microbiome were necessary and sufficient to drive alterations in major proliferation and apoptosis signaling pathways thought to govern tumor development. Overall, our findings support the concept that perturbations in host-microbiota interactions that cause low-grade gut inflammation can promote colon carcinogenesis. Cancer Res; 77(1); 27-40. ©2016 AACR. Topics: Animals; Carboxymethylcellulose Sodium; Cell Transformation, Neoplastic; Colitis; Colonic Neoplasms; Disease Models, Animal; Emulsifying Agents; Food Additives; Gastrointestinal Microbiome; Male; Mice; Mice, Inbred C57BL; Polysorbates | 2017 |
Treatment with novel AP-1 and NF-κB inhibitors restores the colonic endocrine cells to normal levels in rats with DSS-induced colitis.
The aim of this study was to determine the effects of two anti-inflammatory agents on the abnormalities in colonic endocrine cells in dextran sodium sulfate (DSS)-induced colitis. Colitis was induced in male Wistar rats (n=45) using DSS; a further 15 rats without colitis were included in a healthy control group. The animals with DSS-induced colitis were randomly divided into 3 treatment groups as follows: i) DSS group, rats were treated with 0.5 ml of 0.5% carboxymethyl cellulose (CMC); ii) DSS‑G group, rats were treated with 3-[(dodecylthiocarbonyl)‑methyl]‑glutarimide (DTCM‑G), a novel activator protein 1 (AP-1) inhibitor, 20 mg/kg in CMC; and iii) DSS‑Q group, rats were treated with dehydroxymethylepoxyquinomicin, a nuclear factor κB (NF-κB) inhibitor, 15 mg/kg in CMC. The treatments were administered intraperitoneally, twice daily for 5 days, after which the animals were sacrificed and tissue samples from the colon were immunostained for chromogranin A (CgA), serotonin, peptide YY (PYY), enteroglucagon, pancreatic polypeptide (PP), somatostatin, leukocytes, B/T lymphocytes, B lymphocytes, T lymphocytes, macrophages/monocytes and mast cells. The densities of these endocrine and immune cells were quantified by computer‑aided image analysis. The densities of CgA-, serotonin-, PYY- and enteroglucagon-producing cells were significantly higher, and those of PP- and somatostatin-producing cells were significantly lower in the DSS‑G, DSS‑Q and control groups than in the DSS group. The densities of all the immune cells were lower in the DSS‑G, DSS‑Q and control groups than in the DSS group. The densities of all endocrine cell types and immune cells in both the DSS groups treated with anti‑inflammatory agents were restored to control levels. In conclusion, our data demonstrate that there is an interaction between endocrine and immune cells during inflammation. This interaction with subsequent changes in endocrine cells is responsible for the clinical manifestation of colitis symptoms. Topics: Animals; Anti-Inflammatory Agents; Benzamides; Carboxymethylcellulose Sodium; Colitis; Colon; Cyclohexanones; Dextran Sulfate; Disease Models, Animal; Endocrine Cells; Male; NF-kappa B; Piperidones; Rats; Rats, Wistar; Transcription Factor AP-1 | 2016 |
Anti-inflammatory effects of novel AP-1 and NF-κB inhibitors in dextran-sulfate-sodium-induced colitis in rats.
The aim of the present study was to elucidate the anti-inflammatory effects of the two novel anti-inflammatory substances, 3-[(dodecylthiocarbonyl)‑methyl]-glutarimide (DTCM-G) and dehydroxymethylepoxyquinomicin (DHMEQ), on DSS-induced colitis in rats. For this purpose, rats with dextran sulfate sodium (DSS)-induced colitis were randomly divided into 3 groups with 10 animals in each group as follows: i) the control group, which received 0.5 ml of 0.5% carboxymethyl cellulose (CMC; vehicle), ii) rats that received DTCM-G (20 mg/kg body weight in 0.5% CMC; the DTCM-G group), and iii) rats that received DHMEQ (15 mg/kg body weight in 0.5% CMC; the DHMEQ group). The animals were sacrificed after the 5-day treatment period, and tissue samples were taken from their colons and sectioned for histological evaluation. The tissue sections were stained with hematoxylin and eosin, and immunostained for leukocytes, lymphocytes, macrophages/monocytes and mast cells. The disease activity index (DAI), histological grading of colitis, and densities of several types of submucosal immune cells were compared between the controls, and the DTCM-G and DHMEQ groups. The DAI values were significantly lower in both the DTCM-G and DHMEQ groups than in the control group. The total scores for the histological grading of colitis were also significantly lower in the DTCM-G and DHMEQ groups than in the control group. The submucosal densities of leucocytes, lymphocytes, macrophages/monocytes and mast cells were significantly lower in the DTCM-G and DHMEQ groups than in the control group. Our findings indicate that the anti-inflammatory and anticancer effects of DTCM-G and DHMEQ, and the absence of any associated toxicity render them excellent therapeutic candidates for clinical use in the treatment of colitis. Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Benzamides; Carboxymethylcellulose Sodium; Colitis; Colon; Cyclohexanones; Dextran Sulfate; Gene Expression Regulation; Lymphocytes; Macrophages; Male; Mast Cells; Monocytes; NF-kappa B; Piperidones; Rats; Rats, Wistar; Signal Transduction; Transcription Factor AP-1; Treatment Outcome | 2016 |
Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome.
The intestinal tract is inhabited by a large and diverse community of microbes collectively referred to as the gut microbiota. While the gut microbiota provides important benefits to its host, especially in metabolism and immune development, disturbance of the microbiota-host relationship is associated with numerous chronic inflammatory diseases, including inflammatory bowel disease and the group of obesity-associated diseases collectively referred to as metabolic syndrome. A primary means by which the intestine is protected from its microbiota is via multi-layered mucus structures that cover the intestinal surface, thereby allowing the vast majority of gut bacteria to be kept at a safe distance from epithelial cells that line the intestine. Thus, agents that disrupt mucus-bacterial interactions might have the potential to promote diseases associated with gut inflammation. Consequently, it has been hypothesized that emulsifiers, detergent-like molecules that are a ubiquitous component of processed foods and that can increase bacterial translocation across epithelia in vitro, might be promoting the increase in inflammatory bowel disease observed since the mid-twentieth century. Here we report that, in mice, relatively low concentrations of two commonly used emulsifiers, namely carboxymethylcellulose and polysorbate-80, induced low-grade inflammation and obesity/metabolic syndrome in wild-type hosts and promoted robust colitis in mice predisposed to this disorder. Emulsifier-induced metabolic syndrome was associated with microbiota encroachment, altered species composition and increased pro-inflammatory potential. Use of germ-free mice and faecal transplants indicated that such changes in microbiota were necessary and sufficient for both low-grade inflammation and metabolic syndrome. These results support the emerging concept that perturbed host-microbiota interactions resulting in low-grade inflammation can promote adiposity and its associated metabolic effects. Moreover, they suggest that the broad use of emulsifying agents might be contributing to an increased societal incidence of obesity/metabolic syndrome and other chronic inflammatory diseases. Topics: Adiposity; Animals; Carboxymethylcellulose Sodium; Colitis; Diet; Emulsifying Agents; Feces; Female; Gastrointestinal Tract; Germ-Free Life; Inflammation; Intestinal Mucosa; Male; Metabolic Syndrome; Mice; Microbiota; Obesity; Polysorbates | 2015 |
Comparative study on experimental autoimmune pancreatitis and its extrapancreatic involvement in mice.
The objective of the study was to study the relationship between autoimmune pancreatitis (AIP) and colitis in C57BL/6 interleukin 10-deficient (IL-10KO) mice and to compare the extrapancreatic involvement of AIP between IL-10KO and MRL/Mp mice that developed pancreatitis.. Six-week-old female IL-10KO and MRL/Mp mice were injected intraperitoneally with polyinosinic polycytidylic acid (poly I:C) twice weekly for 8 or 12 weeks, respectively. The mice were killed, and the severity of inflammation in the pancreas, colon, liver, bile duct, and salivary gland was assessed using histological scoring systems. T-cell subsets derived from IL-10KO mice with pancreatitis were adoptively transferred into recombination activating gene 2-deficient mice.. Administration of poly I:C induced pancreatitis and accelerated the development of colitis in IL-10KO mice. Pancreatitis was characterized by specific destruction of exocrine glands and the production of various autoantibodies. Involvement of the liver and bile duct was observed in both IL-10KO and MRL/Mp mice, but sialadenitis was present only in MRL/Mp mice. Adoptive transfer of CD4(+) T cells from AIP mice induced pancreatitis in recipient mice.. Pancreatitis in IL-10KO mice resembles human type 1 AIP and is not associated with colitis. Genetic background may affect susceptibility to extrapancreatic involvement in type 1 AIP. Topics: Adoptive Transfer; Animals; Autoantibodies; Autoimmune Diseases; Carboxymethylcellulose Sodium; CD4-Positive T-Lymphocytes; Cholangitis; Colitis; Disease Models, Animal; Exocrine Glands; Female; Hepatitis; Humans; Interferon Inducers; Interleukin-10; Mice; Mice, Inbred MRL lpr; Mice, Knockout; Pancreatitis; Poly I-C; Polylysine; Severity of Illness Index; Sialadenitis | 2012 |
Topical application of glycyrrhizin preparation ameliorates experimentally induced colitis in rats.
To examine the efficacy of glycyrrhizin preparation (GL-p) in the treatment of a rat model of ulcerative colitis (UC).. Experimental colitis was induced by oral administration of dextran sodium sulfate. Rats with colitis were intrarectally administered GL-p or saline. The extent of colitis was evaluated based on body weight gain, colon wet weight, and macroscopic damage score. The expression levels of pro-inflammatory cytokines and chemokines in the inflamed mucosa were measured by cytokine antibody array analysis. The effect of GL-p on myeloperoxidase (MPO) activity in the inflamed mucosa and purified enzyme was assayed.. GL-p treatment significantly ameliorated the extent of colitis compared to sham treatment with saline. Cytokine antibody array analysis showed that GL-p treatment significantly decreased the expression levels of pro-inflammatory cytokines and chemokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor-α, cytokine-induced neutrophil chemoattractant-2, and monocyte chemoattractant protein-1 in the inflamed mucosa. Furthermore, GL-p inhibited the oxidative activity of mucosal and purified MPO.. GL-p enema has a therapeutic effect on experimental colitis in rats and may be useful in the treatment of UC. Topics: Administration, Topical; Animals; Carboxymethylcellulose Sodium; Colitis; Cytokines; Dextran Sulfate; Enema; Glycyrrhizic Acid; Male; Peroxidase; Rats; Rats, Wistar | 2011 |
Oral administration of curcumin emulsified in carboxymethyl cellulose has a potent anti-inflammatory effect in the IL-10 gene-deficient mouse model of IBD.
Curcumin is a tumeric-derived, water-insoluble polyphenol with potential beneficial health effects for humans. It has been shown to have preventive as well as therapeutic effects in chemically induced murine models of colitis. To investigate whether curcumin exerts a similar effect on the spontaneous colitis in interleukin (IL)-10 gene-deficient mice, we gavaged these mice daily for 2 weeks with 200 mg/kg per day curcumin emulsified in carboxymethyl cellulose, a food additive generally used as a viscosity modifier. Mice fed the curcumin/carboxymethyl cellulose mixture and those receiving carboxymethyl cellulose alone demonstrated similar reductions in histological injury score and colon weight/length ratio compared to water-fed controls. However, significant reductions in pro-inflammatory cytokine release in intestinal explant cultures were only seen in mice treated with the curcumin mixture. Our data demonstrate that in IL-10 gene-deficient mice, both oral curcumin and carboxymethyl cellulose, appear to have modifying effects on colitis. However, curcumin has additional anti-inflammatory effects mediated through a reduced production of potent pro-inflammatory mucosal cytokines. Topics: Administration, Oral; Analysis of Variance; Animals; Carboxymethylcellulose Sodium; Colitis; Curcumin; Disease Models, Animal; Emulsions; Enzyme-Linked Immunosorbent Assay; Interferon-gamma; Interleukin-10; Interleukin-17; Mice; Peroxidase | 2010 |