scholarly journals Oral Dextran Sulfate Sodium Administration Induces Peripheral Spondyloarthritis Features in SKG Mice Accompanied by Intestinal Bacterial Translocation and Systemic Th1 and Th17 Cell Activation.

2021 ◽  
Author(s):  
Yuya Tabuchi ◽  
Masao Katsushima ◽  
Yuri Nishida ◽  
Mirei Shirakashi ◽  
Hideaki Tsuji ◽  
...  
Keyword(s):  
Bacterial Translocation ◽  
Whole Blood ◽  
Th17 Cell ◽  
Cell Activation ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Quantitative Polymerase Chain Reaction ◽  
Bacterial Species ◽  
Bacterial Dna ◽  
Anti Fungal

Abstract Background: Spondyloarthritis (SpA) is an autoimmune and autoinflammatory musculoskeletal disease characterised by systemic enthesitis. Recent research has focused on subclinical inflammatory bowel disease (IBD) in SpA pathogenesis. SKG mice, harbouring the Zap70 W163C mutation, increase autoreactive Th17 cells intrinsically, and show SpA features, including enteritis, after peritoneal injection of β-1,3- glucan under SPF conditions. In a conventional environment, they exhibit spontaneous arthritis with fungal factors. This study aimed to clarify whether oral dextran sulfate sodium (DSS) administration, utilised in IBD model mice, can provoke SpA features in SKG mice under SPF conditions, focusing on the relationship between gut microorganisms and SpA pathogenesis.Methods: SKG and BALB/c mice were administered oral DSS, and their body weights, arthritis, and enthesitis scores were recorded. In another cohorts, antibiotics (meropenem and vancomycin) or an anti-fungal agent (amphotericin B) were administered orally before DSS administration. The splenic Th1 and Th17 cell populations were examined before and after DSS administration using flow cytometry. Furthermore, the amount of circulating bacterial DNA in whole blood was measured by absolute quantitative polymerase chain reaction (qPCR), and the number and characteristics of bacterial species corresponding to these circulating DNA were analised by next-generation sequencing (NGS).Results: Ankle enthesitis as a peripheral SpA feature was elicited in half of DSS-administered SKG mice, and none of the BALB/c mice. Pre-administration of antibiotics suppressed enthesitis, whilst an anti-fungal agent could not. Th1 and Th17 cell levels in the spleen increased after DSS administration, and this was suppressed by pre-administration of antibiotics. SKG mice have a larger amount of bacterial DNA in whole blood than BALB/c mice before and one day after the initiation of DSS administration. The number of bacterial species in whole blood increased after DSS administration in SKG and BALB/c mice. Some genera and species significantly specific to the DSS-treated SKG mice group were also detected. Conclusion: Oral DSS administration alone elicited peripheral enthesitis in SKG mice with bacterial translocation accompanied by increased splenic Th1 and Th17 cell levels. Pre-administration of antibiotics ameliorated these DSS-induced SpA features. These findings suggest that intestinal bacterial leakage plays a pivotal role in SpA pathogenesis.

scholarly journals APicrorhiza kurroaDerivative, Picroliv, Attenuates the Development of Dextran-Sulfate-Sodium-Induced Colitis in Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
De-Kui Zhang ◽  
Jian-Jie Yu ◽  
Yu-Min Li ◽  
Li-Na Wei ◽  
Yi Yu ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Quantitative Polymerase Chain Reaction ◽  
Critical Role ◽  
Disease Activity Index ◽  
Enzyme Linked Immunosorbent Assay ◽  
Histological Score ◽  
Polymerase Chain ◽  
Histology Score

Background. Free radicals and proinflammatory cytokines have been shown to play a critical role in the pathogenesis of ulcerative colitis (UC). Picroliv, aPicrorhiza kurroaderivative, has been demonstrated to have antioxidant and anti-inflammatory effect. The purpose of the study was to investigate the effects of picroliv on experimental model of UC in mice.Materials and Methods. Picroliv was administrated orally by gavage to mice with colitis induced by dextran sulfate sodium (DSS). Disease activity index (DAI), colon length, and histology score were observed. Myeloperoxidase (MPO) activity, and SOD, MDA concentrations were measured by enzyme-linked immunosorbent assay (ELISA) while the expression of cytokine mRNAs was studied by real-time-quantitative polymerase chain reaction and also ELISA. The expression of NF-κB p65 was observed by immunohistochemistry staining and western blotting.Results. A significant improvement was observed in DAI and histological score in mice treated with picroliv, and incerased MPO activity, MDA concentrations, and the expression of IL-1β, TNF-α, and NF-κB p65 in mice with DSS-induced colitis were significantly reduced while decreased SOD level increased following administration of picroliv.Conclusion. The administration of picroliv leads to an amelioration of DSS-induced colitis, suggesting administration of picroliv may provide a therapeutic approach for UC.

scholarly journals The Potential of Vitamin D3 to Repaired Mucosal Injury in Dextran Sulfate Sodium Induced Acute Colitis in Mice

2021 ◽  
Vol 9 (B) ◽  
pp. 931-936
Author(s):  
Satrio Wibowo ◽  
Krisni Subandiyah ◽  
Kusworini Handono ◽  
Sri Poeranto
Keyword(s):  
Stem Cell ◽  
Vitamin D3 ◽  
Cell Activation ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Disease Activity Index ◽  
Mucosal Injury ◽  
Potential Effect ◽  
Mucosal Repair

BACKGROUND: Inflammatory Bowel Disease (IBD) has become an emerging disease worldwide. The treatment of IBD involves two basic principles: Inflammation control and mucosal repair. AIM: This study evaluates the potential effect of Vitamin D3 in mucosal repair through colon stem cell activation and proliferation. METHODS: Dextran sulfate sodium (DSS; 5%) was used to induce colitis in mice. Vitamin D3 at various dosages was then administered as a treatment. The mice were divided into five groups: Control (C-); DSS only (C+); and DSS (5%) plus Vitamin D3 at 0.2 μg (VD1), 0.4 μg (VD2), or 0.6 μg (VD3) per 25 g body weight as the treatment groups. Immunofluorescence analyses of Lgr5+ expression indicated stem cell activation, and Ki67 expression indicated stem cell proliferation. The disease activity index (DAI), colon length, and histopathological index scores were determined after treatment to assess the inflammation and severity of colitis. RESULTS: Immunofluorescence analyses showed a gradually increasing expression of Lgr5+ also Ki67 in proportion with high doses group of Vitamin D3 (p < 0.05). The colon length, DAI scores, and histopathological index scores improved in all groups after Vitamin D3 treatment (p = 0.05; p = 0.026; and p = 0.029, respectively). CONCLUSION: Vitamin D3 has a potential beneficial effect on amplifying intestinal stem cells regulated by Wnt/B-catenin signaling. It is also reduced the inflammatory process proved by the evaluation severity of colitis. It might play an essential role in mucosal repair in IBD.

scholarly journals CpG motifs of bacterial DNA exacerbate colitis of dextran sulfate sodium-treated mice

2002 ◽  
Vol 32 (7) ◽  
pp. 2084 ◽  
Author(s):  
Florian Obermeier ◽  
Nadja Dunger ◽  
Ludwig Deml ◽  
Hans Herfarth ◽  
Jürgen Schölmerich ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Bacterial Dna ◽  
Cpg Motifs

scholarly journals Mice Deficient in Cyp4a14 Have An Increased Number of Goblet Cells and Attenuated Dextran Sulfate Sodium-Induced Colitis

2018 ◽  
Vol 50 (6) ◽  
pp. 2272-2282 ◽  
Author(s):  
Qingxia Xuan ◽  
Yunfeng Zhou ◽  
Binbin Tan ◽  
Zhongyue Xiao ◽  
Shizhen Dong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Quantitative Polymerase Chain Reaction ◽  
Periodic Acid ◽  
Mucosal Injury ◽  
Goblet Cells ◽  
Mrna Levels ◽  
Periodic Acid Schiff ◽  
Monooxygenase Activity

Background/Aims: Cyp4a14 is a member of cytochrome P450 (Cyp450) enzyme superfamily that possesses NADPH monooxygenase activity, which catalyzes omega-hydroxylation of medium-chain fatty acids and arachidonic acid. Study suggests that down-regulation of Cyp4a14 has an anti-inflammatory response in intestine. The present study was to test the function of Cyp4a14 in dextran sulfate sodium (DSS)-induced colitis. Methods: Female Cyp4a14-knockout (KO) and wild-type (WT) mice were treated with DSS for 6 days to induce colitis. The colon of mice was histologically observed by hematoxylin and eosin (H&E) and periodic acid Schiff (PAS) staining. The serum malondialdehyde (MDA), an endogenous indicator of oxidative stress, was chemically measured. Proinflammatory and NADPH oxidase genes were examined by quantitative polymerase chain reaction (qPCR). Results: Cyp4a14-KO mice had a significantly higher number of goblet cells in the colon and were more resistant to DSS-induced colitis compared with the WT mice. The DSS-treated KO mice had lower levels of MDA. Consistent with the milder inflammatory pathological changes, DSS-treated KO mice had lower levels of IL-1β, IL-6 and TNF-α mRNA in the liver and the colon. Moreover, the colon of DSS-treated Cyp4a14-KO and WT mice had higher mRNA levels of two members of NADPH oxidases, Nox2 and Nox4, suggesting that both Nox2 and Nox4 are inflammatory markers. By contrast, DSS-treated WT and KO mice had drastically decreased epithelium-localized Nox1 and dual oxidase (Duox) 2 mRNA levels, coinciding with the erosion of the mucosa induced by DSS. Conclusion: These results suggests a hypothesis that the increased goblet cell in the colon of Cyp4a14-KO mice provides protection from mucosal injury and Cyp4a14-increased oxidative stress exacerbates DSS-induced colitis. Therefore, Cyp4a14 may represent a potential target for treating colitis.

Pretreatment and Treatment WithL-Arginine Attenuate Weight Loss and Bacterial Translocation in Dextran Sulfate Sodium Colitis

2016 ◽  
Vol 40 (8) ◽  
pp. 1131-1139 ◽  
Author(s):  
Maria Emília Rabelo Andrade ◽  
Rosana das Graças Carvalho dos Santos ◽  
Anne Danieli Nascimento Soares ◽  
Kátia Anunciação Costa ◽  
Simone Odília Antunes Fernandes ◽  
...  
Keyword(s):  
Weight Loss ◽  
Bacterial Translocation ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium

scholarly journals Low Dose of Cyanidin-3-O-Glucoside Alleviated Dextran Sulfate Sodium–Induced Colitis, Mediated by CD169+ Macrophage Pathway

2019 ◽  
Vol 25 (9) ◽  
pp. 1510-1521 ◽  
Author(s):  
Yuan Xia ◽  
Ling-min Tian ◽  
Yu Liu ◽  
Kang-Shun Guo ◽  
Min Lv ◽  
...  
Keyword(s):  
Fruits And Vegetables ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Quantitative Polymerase Chain Reaction ◽  
Interferon Γ ◽  
Type I ◽  
Type I Ifn ◽  
Mesenteric Lymph Nodes

Abstract Background Inflammatory bowel disease (IBD) is a chronic disease of the intestinal tract in which excessive activation of inflammatory response is correlated. Cyanidin-3-O-glucoside (C3G) is a powerful anti-inflammatory agent, widely existing in fruits and vegetables. However, the role of C3G has rarely been investigated in dextran sulfate sodium (DSS)–induced colitis. Methods In an attempt to elucidate the possible mechanism of IBD and develop new efficient therapeutic methods for colitis, we evaluated the effects of C3G on DSS-induced colitis. DSS-induced colitic C57BL/6 mice were intraperitoneal injected with 1ug C3G or phosphate buffer every 2 days, a total of 3 times; the changes in macrophages and regular T cells were analyzed by flow cytometry and immunofluorescence. Cytokines and chemokines were measured by real-time quantitative polymerase chain reaction. Results The results showed that C3G treatment did not cause changes in body weight and colon length as much as those of DSS-treated mice only. Cytokine expression levels such as interleukin (IL)- 6, IL-1β, IL-18, tumor necrosis factor α, interferon γ (IFN γ) in colons and mesenteric lymph nodes (mLNs) from C3G-treated mice were lower than those from colitic mice. Meanwhile, C3G injection inhibited the decrease in CCL22 levels and Tregs induction in colitic mice. Furthermore, the activation of macrophages by LPS and increase of CD169+ cells induced by type I IFN could be inhibited by C3G directly in vitro. Conclusions The study is the first to demonstrate strong effects of C3G to alleviate DSS-induced colonic damage in mice. The effect of C3G on DSS-induced colitis clearly showed a decrease of CD169+ macrophages in both the colon and mLNs. An increase of CD169+ cells induced by type I IFN could be inhibited by C3G. All these data suggest that the role of C3G in colitic inflammation was mediated at least partially by CD169+ cells and the type I IFN pathway.

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