Sulforaphane attenuates dextran sodium sulphate induced intestinal inflammation via IL-10/STAT3 signaling mediated macrophage phenotype switching

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

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Somatostatin does not attenuate intestinal injury in dextran sodium sulphate-induced subacute colitis

Mediators of Inflammation ◽

10.1080/09629359891108 ◽

1998 ◽

Vol 7 (3) ◽

pp. 169-173 ◽

Cited By ~ 5

Author(s):

J. D. van Bergeijk ◽

M. E. van Meeteren ◽

C. J. A. M. Tak ◽

A. P. M. van Dijk ◽

M. A. C. Meijssen ◽

...

Keyword(s):

Intestinal Inflammation ◽

Experimental Colitis ◽

Sodium Sulphate ◽

Dextran Sodium Sulphate ◽

Acute Colitis ◽

Inflammatory Score ◽

Long Acting ◽

Intestinal Macrophage

From severalin vitroandin vivostudies involvement of som atostatin (SMS) in intestinal inflammation emerge. Acute colitis induced in rats is attenuated by the long-acting SMS analogue octreotide. We studied the potential beneficial effect of SMS on non-acute experimental colitis. BALB/c mice received either saline, SMS-14 (36 or 120 μg daily) or octreotide (3 μg daily) subcutaneously delivered by implant osmotic pumps. A non-acute colitis was induced by administration of dextran sodium sulphate (DSS) 10% in drinking water during 7 days. DSS evoked a mild, superficial pancolitis, most characterized by mucosal ulceration and submucosal influx of neutrophils. Neither SMS-14 nor octreotide reduced mucosal inflammatory score or macroscopical disease activity, although reduction of intestinal levels of interleukin1 β (IL-1 β), IL-6 and IL-10 during DSS was augmented both by SMS and octreotide. A slight increase of neutrophil influx was seen during SMS administration in animals not exposed to DSS. In conclusion, SMS or its long-acting analogue did not reduce intestinal inflammation in non-acute DSS-induced colitis. According to the cytokine profile observed, SMS-14 and octreotide further diminished the reduction of intestinal macrophage and Th2 lymphocyte activity.

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cis-Urocanic Acid Attenuates Acute Dextran Sodium Sulphate-Induced Intestinal Inflammation

PLoS ONE ◽

10.1371/journal.pone.0013676 ◽

2010 ◽

Vol 5 (10) ◽

pp. e13676 ◽

Cited By ~ 14

Author(s):

Eric Albert ◽

John Walker ◽

Aducio Thiesen ◽

Thomas Churchill ◽

Karen Madsen

Keyword(s):

Intestinal Inflammation ◽

Sodium Sulphate ◽

Urocanic Acid ◽

Dextran Sodium Sulphate

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

Journal of Neuroinflammation ◽

10.1186/s12974-020-02062-2 ◽

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.

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Intestinal inflammation induced by dextran sodium sulphate causes liver inflammation and lipid metabolism disfunction in laying hens

Poultry Science ◽

10.1016/j.psj.2019.11.028 ◽

2020 ◽

Vol 99 (3) ◽

pp. 1663-1677

Author(s):

T. Nii ◽

T. Bungo ◽

N. Isobe ◽

Y. Yoshimura

Keyword(s):

Lipid Metabolism ◽

Laying Hens ◽

Intestinal Inflammation ◽

Sodium Sulphate ◽

Liver Inflammation ◽

Dextran Sodium Sulphate

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Neutralization of LIGHT ameliorates acute dextran sodium sulphate-induced intestinal inflammation

Immunology ◽

10.1111/j.1365-2567.2009.03131.x ◽

2009 ◽

Vol 128 (3) ◽

pp. 451-458 ◽

Cited By ~ 15

Author(s):

Michaela Jungbeck ◽

Barbara Daller ◽

Josef Federhofer ◽

Anja K. Wege ◽

Nadin Wimmer ◽

...

Keyword(s):

Intestinal Inflammation ◽

Sodium Sulphate ◽

Dextran Sodium Sulphate

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Dietary fish oil and curcumin combine to modulate colonic cytokinetics and gene expression in dextran sodium sulphate-treated mice

British Journal Of Nutrition ◽

10.1017/s0007114511000390 ◽

2011 ◽

Vol 106 (4) ◽

pp. 519-529 ◽

Cited By ~ 43

Author(s):

Qian Jia ◽

Ivan Ivanov ◽

Zlatomir Z. Zlatev ◽

Robert C. Alaniz ◽

Brad R. Weeks ◽

...

Keyword(s):

Fish Oil ◽

Chronic Inflammation ◽

Survival Data ◽

Intestinal Inflammation ◽

Fatty Acid Content ◽

Mucosal Injury ◽

Sodium Sulphate ◽

Dietary Lipids ◽

Dextran Sodium Sulphate ◽

Chronic Intestinal Inflammation

Both fish oil (FO) and curcumin have potential as anti-tumour and anti-inflammatory agents. To further explore their combined effects on dextran sodium sulphate (DSS)-induced colitis, C57BL/6 mice were randomised to four diets (2 × 2 design) differing in fatty acid content with or without curcumin supplementation (FO, FO+2 % curcumin, maize oil (control, MO) or MO+2 % curcumin). Mice were exposed to one or two cycles of DSS in the drinking-water to induce either acute or chronic intestinal inflammation, respectively. FO-fed mice exposed to the single-cycle DSS treatment exhibited the highest mortality (40 %, seventeen of forty-three) compared with MO with the lowest mortality (3 %, one of twenty-nine) (P = 0·0008). Addition of curcumin to MO increased (P = 0·003) mortality to 37 % compared with the control. Consistent with animal survival data, following the one- or two-cycle DSS treatment, both dietary FO and curcumin promoted mucosal injury/ulceration compared with MO. In contrast, compared with other diets, combined FO and curcumin feeding enhanced the resolution of chronic inflammation and suppressed (P < 0·05) a key inflammatory mediator, NF-κB, in the colon mucosa. Mucosal microarray analysis revealed that dietary FO, curcumin and FO plus curcumin combination differentially modulated the expression of genes induced by DSS treatment. These results suggest that dietary lipids and curcumin interact to regulate mucosal homeostasis and the resolution of chronic inflammation in the colon.

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