scholarly journals Selection strategy of dextran sulfate sodium-induced acute or chronic colitis mouse models based on gut microbial profile

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hao-Ming Xu ◽  
Hong-Li Huang ◽  
Yan-Di Liu ◽  
Jia-Qi Zhu ◽  
You-Lian Zhou ◽  
...  
Keyword(s):  
Drinking Water ◽  
Gut Microbiota ◽  
Relative Abundance ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Chronic Colitis ◽  
Control Groups ◽  
Acute Colitis ◽  
Α Diversity ◽  
Colitis Model

Abstract Background Dextran sulfate sodium (DSS) replicates ulcerative colitis (UC)-like colitis in murine models. However, the microbial characteristics of DSS-triggered colitis require further clarification. To analyze the changes in gut microbiota associated with DSS-induced acute and chronic colitis. Methods Acute colitis was induced in mice by administering 3% DSS for 1 week in the drinking water, and chronic colitis was induced by supplementing drinking water with 2.5% DSS every other week for 5 weeks. Control groups received the same drinking water without DSS supplementation. The histopathological score and length of the colons, and disease activity index (DAI) were evaluated to confirm the presence of experimental colitis. Intestinal microbiota was profiled by 16S rDNA sequencing of cecal content. Results Mice with both acute and chronic DSS-triggered colitis had significantly higher DAI and colon histopathological scores in contrast to the control groups (P < 0.0001, P < 0.0001), and the colon was remarkably shortened (P < 0.0001, P < 0.0001). The gut microbiota α-diversity was partly downregulated in both acute and chronic colitis groups in contrast to their respective control groups (Pielou index P = 0.0022, P = 0.0649; Shannon index P = 0.0022, P = 0.0931). The reduction in the Pielou and Shannon indices were more obvious in mice with acute colitis (P = 0.0022, P = 0.0043). The relative abundance of Bacteroides and Turicibacter was increased (all P < 0.05), while that of Lachnospiraceae, Ruminococcaceae, Ruminiclostridium, Rikenella, Alistipes, Alloprevotella, and Butyricicoccus was significantly decreased after acute DSS induction (all P < 0.05). The relative abundance of Bacteroides, Akkermansia, Helicobacter, Parabacteroides, Erysipelatoclostridium, Turicibacter and Romboutsia was also markedly increased (all P < 0.05), and that of Lachnospiraceae_NK4A136_group, Alistipes, Enterorhabdus, Prevotellaceae_UCG-001, Butyricicoccus, Ruminiclostridium_6, Muribaculum, Ruminococcaceae_NK4A214_group, Family_XIII_UCG-001 and Flavonifractor was significantly decreased after chronic DSS induction (all P < 0.05). Conclusion DSS-induced acute and chronic colitis demonstrated similar symptoms and histopathological changes. The changes in the gut microbiota of the acute colitis model were closer to that observed in UC. The acute colitis model had greater abundance of SCFAs-producing bacteria and lower α-diversity compared to the chronic colitis model.

scholarly journals Editing of the gut microbiota reduces carcinogenesis in mouse models of colitis-associated colorectal cancer

2019 ◽  
Vol 216 (10) ◽  
pp. 2378-2393 ◽  
Author(s):  
Wenhan Zhu ◽  
Naoteru Miyata ◽  
Maria G. Winter ◽  
Alexandre Arenales ◽  
Elizabeth R. Hughes ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Gut Microbiota ◽  
Chronic Inflammation ◽  
Mouse Models ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
E Coli ◽  
Gut Colonization ◽  
Gut Microbiota Dysbiosis ◽  
Colitis Model

Chronic inflammation and gut microbiota dysbiosis, in particular the bloom of genotoxin-producing E. coli strains, are risk factors for the development of colorectal cancer. Here, we sought to determine whether precision editing of gut microbiota metabolism and composition could decrease the risk for tumor development in mouse models of colitis-associated colorectal cancer (CAC). Expansion of experimentally introduced E. coli strains in the azoxymethane/dextran sulfate sodium colitis model was driven by molybdoenzyme-dependent metabolic pathways. Oral administration of sodium tungstate inhibited E. coli molybdoenzymes and selectively decreased gut colonization with genotoxin-producing E. coli and other Enterobacteriaceae. Restricting the bloom of Enterobacteriaceae decreased intestinal inflammation and reduced the incidence of colonic tumors in two models of CAC, the azoxymethane/dextran sulfate sodium colitis model and azoxymethane-treated, Il10-deficient mice. We conclude that metabolic targeting of protumoral Enterobacteriaceae during chronic inflammation is a suitable strategy to prevent the development of malignancies arising from gut microbiota dysbiosis.

scholarly journals Stachyose modulates gut microbiota and alleviates dextran sulfate sodium-induced acute colitis in mice

2020 ◽  
Vol 26 (3) ◽  
pp. 153
Author(s):  
Qing He ◽  
Liwen He ◽  
Feiran Zhang ◽  
Zhengyang Jian ◽  
Jiachen Sun ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Acute Colitis

scholarly journals The potential of a single injection of hUCMSCs in relevant testis injury and related severity of DSS induced acute and chronic colitis

2021 ◽  
Author(s):  
Yu-Lung Chang ◽  
Huei-Yu Lo ◽  
Shun-Ping Cheng ◽  
Kuo-Ting Chang ◽  
Xiu-Fang Lin ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Single Injection ◽  
Testicular Function ◽  
Chronic Colitis ◽  
Acute Colitis ◽  
Function Impairment ◽  
Cell Groups ◽  
Testicular Injury ◽  
Phosphate Buffered Saline

Abstract Background A single injection of human umbilical mesenchymal stem cells (hUCMSCs) can improve dextran sulfate sodium (DSS)–induced acute colitis and decrease progression of acute to chronic colitis. We report the therapeutic efficacy of hUCMSCs in acute and chronic colitis-related testicular injury. Methods Male C57BL/6JNarl mice were divided into control, phosphate-buffered saline 1 (PBS1), PBS2, hUCMSCs 1 (SC1), and SC2 treated groups. Colitis were induced in the mice using 3% DSS. The mice in the SC1 and SC2 groups underwent a single injection of hUCMSCs. Results The ratio of spermatogenesis impairment of mice in the stem cell groups was lower than that in the PBS groups on days 8 and 25 (P=.029, .043). The overall testicular function impairment and severity of colitis in the PBS2 group were lower than those in the PBS1 group on days 8 and 25 (P=.031, .016). The overall testicular function impairment and severity of colitis in the SC2 group were lower than those in the SC1 group on days 8 and 25 (P=.031, .016). Conclusions Disease activity of acute colitis is a good predictor of severity and prognosis of testicular injury in mice with colitis. hUCMSCs can reduce the ratio of testicular function impairment in acute and chronic colitis.

scholarly journals Selenium-Enriched Lactobacillus acidophilus Ameliorates Dextran Sulfate Sodium-Induced Chronic Colitis in Mice by Regulating Inflammatory Cytokines and Intestinal Microbiota

2021 ◽  
Vol 8 ◽  
Author(s):  
Zeyu Wu ◽  
Dan Pan ◽  
Min Jiang ◽  
Lixuan Sang ◽  
Bing Chang
Keyword(s):  
Inflammatory Cytokines ◽  
Intestinal Microbiota ◽  
Relative Abundance ◽  
Lactobacillus Acidophilus ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Disease Activity Index ◽  
Chronic Colitis ◽  
Group A

Aim: To evaluate the effect of Selenium-enriched Lactobacillus acidophilus (Se-enriched L. acidophilus) on dextran sulfate sodium (DSS)-induced colitis in mice.Methods: Mice were randomly divided into four groups: a control group, a control + Se-enriched L. acidophilus group, a chronic colitis group, and a chronic colitis + Se-enriched L. acidophilus group (n = 10 each group). The mice were sacrificed on the 26th day. The disease activity index, survival rates, and histological injury score were determined. Cytokines produced by lamina propria lymphocytes (LPLs), the selenium (Se) concentrations in serum and colon tissue and the mouse intestinal microbiota were evaluated.Results: Se-enriched L. acidophilus can improve histological injury and the disease activity index in mice with chronic colitis and reduce IL-1β, IL-6, IL-12p70, TNF-α, IL-23, IFN-γ, IL-17A, and IL-21 (P &lt; 0.05) and increase IL-10 (P &lt; 0.05) expression levels. Moreover, Se-enriched L. acidophilus can increase the β diversity of intestinal microbiota in mice with chronic colitis, significantly reduce the relative abundance of Lactobacillus and Romboutsia (P &lt; 0.05), and significantly increase the relative abundance of Parasutterella (P &lt; 0.05).Conclusions: Se-enriched L. acidophilus can improve DSS-induced chronic colitis by regulating inflammatory cytokines and intestinal microbiota.

scholarly journals Akkermansia muciniphila Alleviates Dextran Sulfate Sodium (DSS)-Induced Acute Colitis by NLRP3 Activation

2021 ◽  
Author(s):  
Siwen Qu ◽  
Lina Fan ◽  
Yadong Qi ◽  
Chaochao Xu ◽  
Yingying Hu ◽  
...  
Keyword(s):  
Immune Response ◽  
Gut Microbiota ◽  
Inflammatory Disease ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Underlying Mechanism ◽  
Acute Colitis ◽  
Content Type ◽  
Akkermansia Muciniphila ◽  
Intestinal Inflammatory Disease

The gut microbiota and host immune response interaction influences the progression of intestinal inflammatory disease. As a well-recognized next-generation probiotic, Akkermansia muciniphila has been proved to play a crucial role in the progression of colitis, but its underlying mechanism remains inconclusive.

scholarly journals Nicotinamide Ameliorates Dextran Sulfate Sodium-Induced Chronic Colitis in Mice through Its Anti-Inflammatory Properties and Modulates the Gut Microbiota

2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Kai Kang ◽  
Yue Sun ◽  
Dan Pan ◽  
Bing Chang ◽  
Li-Xuan Sang
Keyword(s):  
Gut Microbiota ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Alpha Diversity ◽  
Short Chain Fatty Acids ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Chronic Colitis ◽  
Anti Inflammatory

Vitamin B (nicotinamide (NAM)), one of the most important nutritional components for humans, exerts anti-inflammatory activity. This study was aimed at investigating the effect of NAM on the gut microbiota and short-chain fatty acids (SCFAs) in mice with chronic colitis. Colitis was induced in C57BL/6 male mice by administration of 1.5% dextran sulfate sodium (DSS), and the mice were intraperitoneally injected with normal saline (NS) or NAM. NAM treatment ameliorated weight loss and changes in colon length, disease activity index (DAI) score, and histologic scores. Moreover, enzyme-linked immunosorbent assay (ELISA) analysis of LPL cells revealed that the level of interleukin- (IL-) 6, IL-12p70, IL-1β, tumor necrosis factor- (TNF-) α, interferon- (IFN-) γ, IL-21, and IL-17A was increased, while IL-10 was reduced, in the chronic colitis group compared to the control group, but the levels of all these factors were restored after NAM treatment. Then, 16S rRNA sequencing of the large intestinal content was performed, and analysis of alpha diversity and beta diversity showed that the richness of the gut microbiota was decreased in the DSS group compared to the control group and restored after NAM treatment. In addition, NAM modulated specific bacteria, including Odoribacter, Flexispira, and Bifidobacterium, in the NAM+chronic colitis group. Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt) analysis indicated that NAM treatment restored disruptions in the functions of the gut microbiota (replication and repair, cell motility) in mice with DSS-induced colitis. Furthermore, NAM also restored the reduction in valeric acid in mice with DSS-induced chronic colitis. Our results suggest that NAM treatment could alleviate DSS-induced chronic colitis in mice by inhibiting inflammation and regulating the composition and function of gut microbiota.

scholarly journals Dietary Interventions to Prevent High Fructose Diet-associated Worsening of Colitis and Colitis-associated Tumorigenesis in Mice

2021 ◽  
Author(s):  
Ryohei Nishiguchi ◽  
Srijani Basu ◽  
Hannah A Staab ◽  
Naotake Ito ◽  
Xi Kathy Zhou ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Control Diet ◽  
Experimental Colitis ◽  
Protective Effects ◽  
Diet Change ◽  
Chronic Colitis ◽  
Acute Colitis ◽  
High Fructose Diet ◽  
High Consumption ◽  
High Fructose

Abstract Diet is believed to be an important factor in the pathogenesis of Inflammatory Bowel Disease. High consumption of dietary fructose has been shown to exacerbate experimental colitis, an effect mediated through the gut microbiota. This study evaluated whether dietary alterations could attenuate the detrimental effects of a high fructose diet (HFrD) in experimental colitis. First, we determined whether the pro-colitic effects of a HFrD could be reversed by switching mice from a HFrD to a control diet. This diet change completely prevented HFrD-induced worsening of acute colitis, in association with a rapid normalization of the microbiota. Second, we tested the effects of dietary fiber, which demonstrated that psyllium was the most effective type of fiber for protecting against HFrD-induced worsening of acute colitis, compared to pectin, inulin or cellulose. In fact, supplemental psyllium nearly completely prevented the detrimental effects of the HFrD, an effect associated with a shift in the gut microbiota. We next determined whether the protective effects of these interventions could be extended to chronic colitis and colitis-associated tumorigenesis. Using the azoxymethane/dextran sodium sulfate model, we first demonstrated that HFrD feeding exacerbated chronic colitis and increased colitis-associated tumorigenesis. Using the same dietary changes tested in the acute colitis setting, we also showed that mice were protected from HFrD-mediated enhanced chronic colitis and tumorigenesis, upon either diet switching or psyllium supplementation. Taken together, these findings suggest that high consumption of fructose may enhance colon tumorigenesis associated with long-standing colitis, an effect that could be reduced by dietary alterations.

scholarly journals Acetylcholine-producing T cells augment innate immune-driven colitis but are redundant in T cell-driven colitis

2019 ◽  
Vol 317 (5) ◽  
pp. G557-G568 ◽  
Author(s):  
Rose A. Willemze ◽  
David J. Brinkman ◽  
Olaf Welting ◽  
Patricia H. P. van Hamersveld ◽  
Caroline Verseijden ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Inflammatory Cytokine ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Innate Immune ◽  
Cytokine Levels ◽  
Colitis Model

Clinical trials suggest that vagus nerve stimulation presents an alternative approach to classical immune suppression in Crohn's disease. T cells capable of producing acetylcholine (ChAT+ T cells) in the spleen are essential mediators of the anti-inflammatory effect of vagus nerve stimulation. Besides the spleen, ChAT+ T cells are found abundantly in Peyer’s patches of the small intestine. However, the role of ChAT+ T cells in colitis pathogenesis is unknown. Here, we made use of CD4creChATfl/fl mice (CD4ChAT−/− mice) lacking ChAT expression specifically in CD4+ T cells. Littermates (ChATfl/fl mice) served as controls. In acute dextran sulfate sodium (DSS)-induced colitis (7 days of 2% DSS in drinking water), CD4ChAT−/− mice showed attenuated colitis and lower intestinal inflammatory cytokine levels compared with ChATfl/fl mice. In contrast, in a resolution model of DSS-induced colitis (5 days of 2% DSS followed by 7 days without DSS), CD4ChAT−/− mice demonstrated a worsened colitis recovery and augmented colonic histological inflammation scores and inflammatory cytokine levels as compared with ChATfl/fl mice. In a transfer colitis model using CD4+CD45RBhigh T cells, T cells from CD4ChAT−/− mice induced a similar level of colitis compared with ChATfl/fl T cells. Together, our results indicate that ChAT+ T cells aggravate the acute innate immune response upon mucosal barrier disruption in an acute DSS-induced colitis model, whereas they are supporting the later resolution process of this innate immune-driven colitis. Surprisingly, ChAT expression in T cells seems redundant in the context of T cell-driven colitis. NEW & NOTEWORTHY By using different mouse models of experimental colitis, we provide evidence that in dextran sulfate sodium-induced colitis, ChAT+ T cells capable of producing acetylcholine worsen the acute immune response, whereas they support the later healing phase of this innate immune-driven colitis.

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