scholarly journals Oral Ferric Maltol Does Not Adversely Affect the Intestinal Microbiome of Patients or Mice, But Ferrous Sulphate Does

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2269
Author(s):  
Awad Mahalhal ◽  
Alessandra Frau ◽  
Michael D. Burkitt ◽  
Umer Z. Ijaz ◽  
Christopher A. Lamb ◽  
...  
Keyword(s):  
Ferrous Sulphate ◽  
Sodium Sulphate ◽  
Intestinal Microbiome ◽  
Dextran Sodium Sulphate ◽  
Principal Coordinates Analysis ◽  
Statistical Inferences ◽  
Principal Coordinates ◽  
Inflammatory Bowel ◽  
The Impact ◽  
Measurable Change

Background and Aims: Altering dietary ferrous sulphate (FS) consumption exacerbates a murine model of colitis and alters the intestinal microbiome. We investigated the impact of oral ferric maltol (FM) and FS on mice with dextran sodium sulphate (DSS) induced colitis, and the microbiome of patients with iron deficiency. Methods: Mice had acute colitis induced, with 2% DSS for 5 days, followed by water. During this period, groups of mice were fed standard chow (200 ppm iron, SC, n = 8), or SC with 200ppm FS supplementation (n = 16, FSS), or SC with 200 ppm FM supplementation (n = 16, FMS). Clinical, pathological and microbiome assessments were compared at days 1 and 10. Fecal bacterial gDNA was extracted and the microbiome assessed by sequencing. Statistical inferences were made using MacQIIME. Principal Coordinates Analysis were used to visualize beta-diversity cluster analysis. Ten patients with IDA were treated with FS, and six with inactive inflammatory bowel disease received FM, supplements for four weeks: pre- and mid-treatment fecal samples were collected: the microbiome was assessed (see above). Results: In mice, after DSS treatment, there was a decrease in many genera in the SC and FSS groups: Lactobacillales increased in mice that received FMS. In humans, FS treatment led to an increase in five genera, but FM was not associated with any measurable change. The severity of DSS-induced colitis was greater with FSS than FMS. Conclusions: This study demonstrates differential and unique influences of ferric maltol and ferrous sulphate supplements on intestinal microbiota. These differences might contribute to the different side effects associated with these preparations.

scholarly journals Dietary folate does not significantly affect the intestinal microbiome, inflammation or tumorigenesis in azoxymethane–dextran sodium sulphate-treated mice

2012 ◽  
Vol 109 (4) ◽  
pp. 630-638 ◽  
Author(s):  
Amanda J. MacFarlane ◽  
Nathalie A. Behan ◽  
Fernando M. G. Matias ◽  
Judy Green ◽  
Don Caldwell ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Distal Colon ◽  
Sodium Sulphate ◽  
Intestinal Microbiome ◽  
Dextran Sodium Sulphate ◽  
Dietary Folate ◽  
Chemically Induced ◽  
Inflammatory Bowel ◽  
Tumour Initiation ◽  
The Impact

Inflammatory bowel disease (IBD) is a risk factor for the development of colon cancer. Environmental factors including diet and the microflora influence disease outcome. Folate and homocysteine have been associated with IBD-mediated colon cancer but their roles remain unclear. We used a model of chemically induced ulcerative colitis (dextran sodium sulphate (DSS)) with or without the colon carcinogen azoxymethane (AOM) to determine the impact of dietary folic acid (FA) on colonic microflora and the development of colon tumours. Male mice (n 15 per group) were fed a FA-deficient (0 mg/kg), control (2 mg/kg) or FA-supplemented (8 mg/kg) diet for 12 weeks. Folate status was dependent on the diet (P< 0·001) and colitis-induced treatment (P= 0·04) such that mice with colitis had lower circulating folate. FA had a minimal effect on tumour initiation, growth and progression, although FA-containing diets tended to be associated with a higher tumour prevalence in DSS-treated mice (7–20 v. 0 %, P= 0·08) and the development of more tumours in the distal colon of AOM-treated mice (13–83 % increase, P= 0·09). Folate deficiency was associated with hyperhomocysteinaemia (P< 0·001) but homocysteine negatively correlated with tumour number (r − 0·58, P= 0·02) and load (r − 0·57, P= 0·02). FA had no effect on the intestinal microflora. The present data indicate that FA intake has no or little effect on IBD or IBD-mediated colon cancer in this model and that hyperhomocysteinaemia is a biomarker of dietary status and malabsorption rather than a cause of IBD-mediated colon cancer.

scholarly journals Titanium Dioxide Presents a Different Profile in Dextran Sodium Sulphate-Induced Experimental Colitis in Mice Lacking the IBD Risk Gene Ptpn2 in Myeloid Cells

2021 ◽  
Vol 22 (2) ◽  
pp. 772
Author(s):  
Javier Conde ◽  
Marlene Schwarzfischer ◽  
Egle Katkeviciute ◽  
Janine Häfliger ◽  
Anna Niechcial ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Titanium Dioxide ◽  
Genetic Risk ◽  
Intestinal Inflammation ◽  
Sodium Sulphate ◽  
Food Additive ◽  
Wild Type ◽  
Dextran Sodium Sulphate ◽  
Risk Gene ◽  
The Impact

Environmental and genetic factors have been demonstrated to contribute to the development of inflammatory bowel disease (IBD). Recent studies suggested that the food additive; titanium dioxide (TiO2) might play a causative role in the disease. Therefore, in the present study we aimed to explore the interaction between the food additive TiO2 and the well-characterized IBD risk gene protein tyrosine phosphatase non-receptor type 2 (Ptpn2) and their role in the development of intestinal inflammation. Dextran sodium sulphate (DSS)-induced acute colitis was performed in mice lacking the expression of Ptpn2 in myeloid cells (Ptpn2LysMCre) or their wild type littermates (Ptpn2fl/fl) and exposed to the microparticle TiO2. The impact of Ptpn2 on TiO2 signalling pathways and TiO2-induced IL-1β and IL-10 levels were studied using bone marrow-derived macrophages (BMDMs). Ptpn2LysMCre exposed to TiO2 exhibited more severe intestinal inflammation than their wild type counterparts. This effect was likely due to the impact of TiO2 on the differentiation of intestinal macrophages, suppressing the number of anti-inflammatory macrophages in Ptpn2 deficient mice. Moreover, we also found that TiO2 was able to induce the secretion of IL-1β via mitogen-activated proteins kinases (MAPKs) and to repress the expression of IL-10 in bone marrow-derived macrophages via MAPK-independent pathways. This is the first evidence of the cooperation between the genetic risk factor Ptpn2 and the environmental factor TiO2 in the regulation of intestinal inflammation. The results presented here suggest that the ingestion of certain industrial compounds should be taken into account, especially in individuals with increased genetic risk

scholarly journals Effect of Quercetin Monoglycosides on Oxidative Stress and Gut Microbiota Diversity in Mice with Dextran Sodium Sulphate-Induced Colitis

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Zhu Hong ◽  
Meiyu Piao
Keyword(s):  
Oxidative Stress ◽  
Body Weight Gain ◽  
Sodium Sulphate ◽  
The Body ◽  
Control Group ◽  
Simpson Index ◽  
Dextran Sodium Sulphate ◽  
Related Factors ◽  
Inflammatory Bowel ◽  
Quercetin Aglycone

The pathogenesis of inflammatory bowel disease (IBD) is linked to an intricate association of environmental, microbial, and host-related factors. This study examined the potential effects of dietary addition of two preparations from onion, one comprising quercetin aglycone alone (Q: 0.15% polyphenols, quercetin aglycone:quercetin monoglycosides, 98:2) and another comprising quercetin aglycone with monoglycosides (Q+MQ: 0.15% total polyphenols, quercetin aglycone:quercetin monoglycosides, 69:31), on dextran sodium sulphate- (DSS-) induced colitis in mice. The results revealed a significant decrease in the body weight gain of the mice with DSS-induced colitis, which was counteracted by the dietary Q or Q+MQ supplementation. Meanwhile, the oxidative stress indicated by myeloperoxidase (MPO), reduced glutathione (GSH), malondialdehyde (MDA), and serum nitrate (NO) concentrations was higher in mice with DSS-induced colitis than in the control group mice, but dietary Q or Q+MQ supplementation counteracted this trend. The colitis mice demonstrated reduced Chao1, angiotensin-converting enzyme (ACE), and Shannon indices and an increased Simpson index, but the colitis mice receiving dietary Q or Q+MQ exhibited higher Chao1, ACE, and Shannon indices and a reduced Simpson index. In conclusion, this research showed that even at a low dose, dietary Q or Q+MQ supplementation counteracts DSS-induced colitis in mice, indicating that Q or Q+MQ may be used as an adjuvant therapy for IBD patients.

scholarly journals The Effect of Lactobacillus casei on Experimental Porcine Inflammatory Bowel Disease Induced by Dextran Sodium Sulphate

2021 ◽  
Vol 64 (2) ◽  
pp. 85-90
Author(s):  
Jan Bureš ◽  
Darina Kohoutová ◽  
Jaroslav Květina ◽  
Věra Radochová ◽  
Michal Pavlík ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Transverse Colon ◽  
Lactobacillus Casei ◽  
Statistical Significance ◽  
Probiotic Strain ◽  
Sodium Sulphate ◽  
Dextran Sodium Sulphate ◽  
Inflammatory Bowel ◽  
Histopathological Score

Background: Gastrointestinal injury caused by dextran sodium sulphate (DSS) is a reliable porcine experimental model of inflammatory bowel disease (IBD). The purpose of this study was to evaluate the effect of probiotic Lactobacillus casei DN 114001 (LC) on DSS-induced experimental IBD.Results: Eighteen female pigs (Sus scrofa f. domestica, weight 33–36 kg, age 4–5 months) were divided into 3 groups (6 animals per group): controls with no treatment, DSS, and DSS + LC. LC was administered to overnight fasting animals in a dietary bolus in the morning on days 1–7 (4.5 × 1010 live bacteria/day). DSS was applied simultaneously on days 3–7 (0.25 g/kg/day). On day 8, the pigs were sacrificed. Histopathological score and length of crypts/glands (stomach, jejunum, ileum, transverse colon), length and width of villi (jejunum, ileum), and mitotic and apoptotic indices (jejunum, ileum, transverse colon) were assessed. DSS increased the length of glands in the stomach, length of crypts and villi in the jejunum and ileum, and the histopathological score of gastrointestinal damage, length of crypts and mitotic activity in the transverse colon. Other changes did not achieve any statistical significance. Administration of LC reduced the length of villi in the jejunum and ileum to control levels and decreased the length of crypts in the jejunum. Conclusions: Treatment with a probiotic strain of LC significantly accelerated regeneration of the small intestine in a DSS-induced experimental porcine model of IBD.

scholarly journals Dextran Sodium Sulphate Colitis Mouse Model: Traps and Tricks

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Martina Perše ◽  
Anton Cerar
Keyword(s):  
Inflammatory Bowel Disease ◽  
Animal Models ◽  
Bowel Disease ◽  
Sodium Sulphate ◽  
Unknown Etiology ◽  
Dextran Sulphate ◽  
Dextran Sodium Sulphate ◽  
Wide Range ◽  
Inflammatory Bowel ◽  
Colitis Model

Inflammatory bowel disease (IBD) is a complex multifactorial disease of unknown etiology. Thus, dozens of different animal models of IBD have been developed in past decades. Animal models of IBD are valuable and indispensable tools that provide a wide range of options for investigating involvement of various factors into the pathogenesis of IBD and to evaluate different therapeutic options. However, the dextran sulphate sodium (DSS-) induced colitis model has some advantages when compared to other animal models of colitis. It is well appreciated and widely used model of inflammatory bowel disease because of its simplicity. It has many similarities to human IBD, which are mentioned in the paper. In spite of its simplicity and wide applicability, there are also traps that need to be taken into account when using DSS model. As demonstrated in the present paper, various factors may affect susceptibility to DSS-induced lesions and modify results.

scholarly journals The Impact of NOD2 Genetic Variants on the Gut Mycobiota in Crohn’s Disease Patients in Remission and in Individuals Without Gastrointestinal Inflammation

2020 ◽  
Author(s):  
Andrew Nelson ◽  
Christopher J Stewart ◽  
Nicholas A Kennedy ◽  
John K Lodge ◽  
Mark Tremelling ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Relative Abundance ◽  
Mucosal Inflammation ◽  
Rrna Gene ◽  
Wild Type ◽  
Candida Spp ◽  
Principal Coordinates Analysis ◽  
Principal Coordinates ◽  
The Impact

Abstract Background and Aims Historical and emerging data implicate fungi in Crohn’s disease [CD] pathogenesis. However, a causal link between mycobiota, dysregulated immunity, and any impact of NOD2 variants remains elusive. This study aims to evaluate associations between NOD2 variants and faecal mycobiota in CD patients and non-CD subjects. Methods Faecal samples were obtained from 34 CD patients [18 NOD2 mutant, 16 NOD2 wild-type] identified from the UK IBD Genetics Consortium. To avoid confounding influence of mucosal inflammation, CD patients were in clinical remission and had a faecal calprotectin &lt;250 μg/g; 47 non-CD subjects were included as comparator groups, including 22 matched household [four NOD2 mutant] and 25 non-household subjects with known NOD2 genotype [14 NOD2 mutant] identified by the NIHR BioResource Cambridge. Faecal mycobiota composition was determined using internal transcribed spacer 1 [ITS1] sequencing and was compared with 16S rRNA gene sequences and volatile organic compounds. Results CD was associated with higher numbers of fungal observed taxonomic units [OTUs] [p = 0.033]. Principal coordinates analysis using Jaccard index [p = 0.018] and weighted Bray-Curtis dissimilarities [p = 0.01] showed Candida spp. clustered closer to CD patients whereas Cryptococcus spp. clustered closer to non-CD. In CD, we found higher relative abundance of Ascomycota [p = 0.001] and lower relative abundance Basidiomycota [p = 0.019] phyla. An inverse relationship was found between bacterial and fungal Shannon diversity in NOD2 wild-type which was independent of CD [r = -0.349; p = 0.029]. Conclusions This study confirms compositional changes in the gut mycobiota in CD and provides evidence that fungi may play a role in CD pathogenesis. No NOD2 genotype-specific differences were observed in the faecal mycobiota.

scholarly journals Dietary supplementation of Thai black rice bran extract and yeast beta-glucan protects the dextran sodium sulphate mediated colitis induced rat

RSC Advances ◽  
2017 ◽  
Vol 7 (1) ◽  
pp. 396-402 ◽  
Author(s):  
Noppawat Pengkumsri ◽  
Bhagavathi Sundaram Sivamaruthi ◽  
Sasithorn Sirilun ◽  
Prasit Suwannalert ◽  
Teerapat Rodboon ◽  
...  
Keyword(s):  
Rice Bran ◽  
Rat Model ◽  
Sodium Sulfate ◽  
Dietary Supplementation ◽  
Sodium Sulphate ◽  
Black Rice ◽  
Dextran Sodium Sulphate ◽  
Beta Glucan ◽  
Black Rice Bran ◽  
The Impact

The present study was employed to evaluate the impact of black rice bran (RB) extract, and yeast β-glucan (YBG) supplementation on a dextran sodium sulfate (DSS)-induced colitis rat model.

scholarly journals The impact of dextran sodium sulphate and probiotic pre-treatment in a murine model of Parkinson’s disease

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Zach Dwyer ◽  
Melany Chaiquin ◽  
Jeffrey Landrigan ◽  
Kiara Ayoub ◽  
Pragya Shail ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Murine Model ◽  
Gut Microbiome ◽  
Intestinal Inflammation ◽  
Sodium Sulphate ◽  
Dopamine Neurons ◽  
Dextran Sodium Sulphate ◽  
Pre Treatment ◽  
The Impact

Abstract Background Recent work has established that Parkinson’s disease (PD) patients have an altered gut microbiome, along with signs of intestinal inflammation. This could help explain the high degree of gastric disturbances in PD patients, as well as potentially be linked to the migration of peripheral inflammatory factors into the brain. To our knowledge, this is the first study to examine microbiome alteration prior to the induction of a PD murine model. Methods We presently assessed whether pre-treatment with the probiotic, VSL #3, or the inflammatory inducer, dextran sodium sulphate (DSS), would influence the PD-like pathology provoked by a dual hit toxin model using lipopolysaccharide (LPS) and paraquat exposure. Results While VSL #3 has been reported to have anti-inflammatory effects, DSS is often used as a model of colitis because of the gut inflammation and the breach of the intestinal barrier that it induces. We found that VSL#3 did not have any significant effects (beyond a blunting of LPS paraquat-induced weight loss). However, the DSS treatment caused marked changes in the gut microbiome and was also associated with augmented behavioral and inflammatory outcomes. In fact, DSS markedly increased taxa belonging to the Bacteroidaceae and Porphyromonadaceae families but reduced those from Rikencellaceae and S24-7, as well as provoking colonic pro-inflammatory cytokine expression, consistent with an inflamed gut. The DSS also increased the impact of LPS plus paraquat upon microglial morphology, along with circulating lipocalin-2 (neutrophil marker) and IL-6. Yet, neither DSS nor VSL#3 influenced the loss of substantia nigra dopamine neurons or the astrocytic and cytoskeleton remodeling protein changes that were provoked by the LPS followed by paraquat treatment. Conclusions These data suggest that disruption of the intestinal integrity and the associated microbiome can interact with systemic inflammatory events to promote widespread brain-gut changes that could be relevant for PD and at the very least, suggestive of novel neuro-immune communication.

scholarly journals Minor alterations in the intestinal microbiota composition upon Rotavirus infection do not affect susceptibility to DSS colitis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kedir Hussen Hamza ◽  
Emma Dunér ◽  
Isabel Ulmert ◽  
Armando Arias ◽  
Daniel Sorobetea ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Intestinal Barrier ◽  
Intestinal Microbiome ◽  
Enteric Infection ◽  
Intestinal Integrity ◽  
Dss Colitis ◽  
Causative Factors ◽  
Intestinal Immune System ◽  
Inflammatory Bowel ◽  
The Impact

AbstractViral triggers at the intestinal mucosa can have multiple global effects on intestinal integrity, causing elevated intestinal barrier strength and relative protection from subsequent inflammatory bowel disease (IBD) induction in various models. As viruses can interfere with the intestinal immune system both directly and indirectly through commensal bacteria, cause-effect relationships are difficult to define. Due to the complexity of putatively causative factors, our understanding of such virus-mediated protection is currently very limited. We here set out to better understand the impact that adult enteric infection with rotavirus (RV) might have on the composition of the intestinal microbiome and on the severity of IBD. We found that RV infection neither induced significant long-lasting microbiota community changes in the small or large intestine nor affected the severity of subsequent dextran sulfate sodium-induced colitis. Hence, adult murine RV infection does not exert lasting effects on intestinal homeostasis.

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