Comparative analysis of colonic gene expression of three experimental colitis models mimicking inflammatory bowel disease

Velde, Anje A. te; Kort, Floor de; Sterrenburg, Ellen; Pronk, Inge; Kate, Fiebo J.W. ten; Hommes, Daniël W.; Deventer, S. J. H. Van

doi:10.1002/ibd.20079

Cited by 141 publications

(140 citation statements)

References 60 publications

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“…Overexpression of pancreatitis-associated protein (Pap) was detected in the colonic mucosa of IBD patients and DSSinduced colitic mice (Ogawa et al, 2003). Additionally, gene members of the S-100 calcium binding protein family, endogenous activators of innate immune responses, overexpressed in IBD patients were increased, like the previously reports (Lawrance et al, 2001;Dieckgraefe et al, 2002;te Velde et al, 2007). Treatment with C-mix reduced Pap, S100a8 and S100a9 expression.…”

supporting

confidence: 66%

Evaluation of Anti-Colitic Effect of Chung-Jang-Hwan (C-mix) in Mice

Lee¹,

Ahn²,

Park³

et al. 2011

Biomolecules and Therapeutics

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The inhibitory effect of Chung-Jang-Hwan (C-mix) consisted of Geranium nepalense subsp. thunbergii, Saururus chinensis, and Rubus coreanus were investigated in dextran sulfate sodium (DSS)-induced colitic mice by microarray analysis. Treatment with Cmix improved colitic symptoms, including colon shortening and myeloperoxidase activity. Treatment with DSS alone upregulated the expression levels of infl ammation-related genes, including IL-1β, CCL2, CCL4, CCL5, CCL7, CCL8, CCL24, CXCL1, CXCL2, CXCL5, CXCL9 and CXCL10, and other colitis-related genes such as COX-2, PAP, MMP family, S100a8, S100a9 and DEFA1 in mice. However, treatment with C-mix inhibited the expression levels of infl ammation-associated genes induced by DSS. The increased expression levels of COX-2 and IL-1β, representative infl ammatory genes, were confi rmed by a quantitative realtime polymerase chain reaction analysis. These results indicate that C-mix may ameliorate colitis by the inhibitory regulation of infl ammation-associated genes. 52-58 (2011) www.biomolther.org Abstract

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supporting

confidence: 66%

Evaluation of Anti-Colitic Effect of Chung-Jang-Hwan (C-mix) in Mice

Lee¹,

Ahn²,

Park³

et al. 2011

Biomolecules and Therapeutics

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“…Animals were randomized into five groups, each consisting of eight animals, including the control, the dextran sulfate sodium (DSS, MP Biomedicals, USA), the propylene glycol, the triptolide (TL, Zelang Medical Science and Technology Co., Ltd. Nanjing, China), and the dexamethasone groups. Following methods of Stevceva et al (Stevceva et al, 2001, te Velde et al, 2007, all animals were provided free access to 5% DSS solution (5 g DSS in 100 mL distilled water) for seven days, except for the control group that had access to distilled water only. From the third to the seventh day, mice in the propylene glycol group were administered with 2% propylene glycol [0.2 mL, intraperitoneal (ip), quantum dot (qd) injection], the triptolide group was administered 0.6 mg/kg TL in 2% propylene glycol (0.2 mL, ip, qd), and the dexamethasone group was administered 0.4 mg/kg dexamethasone (0.2 mL, ip, qd).…”

Section: Animals and Groupingmentioning

confidence: 99%

Effect of secondary lymphoid tissue chemokine suppression on experimental ulcerative colitis in mice

Zhang

Ding

et al. 2014

Genet. Mol. Res.

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ABSTRACT. The secondary lymphoid tissue chemokine (CCL21) is closely associated with lymphoid homing and anti-tumor immune responses. CCL21 also has a chemotactic effect on intestinal lymphocytes. This study mainly focused on CCL21 expression in experimental ulcerative colitis and on the effects of CCL21 suppression on this disease in mice. The mouse colitis model was induced by dextran sulfate sodium (DSS) in 40 female BALB/c mice that were equally distributed into five groups: control, DSS, propylene glycol, triptolide (TL), and dexamethasone treatment groups. The disease activity index, general morphology score of the colon, and histological pathology score of colon tissues were evaluated. CCL21 expression was examined in colons of mice by immunohistochemistry, reverse transcription-polymerase chain reaction, and Western blotting analysis. CCL21 was upregulated in the mouse model of ulcerative colitis (control group vs DSS group/ propylene glycol group, P < 0.01). The TL and dexamethasone treatments improved colitis symptoms and decreased CCL21 expression (TL group/dexamethasone group vs DSS group/ propylene glycol group, P < 0.05). In conclusion, CCL21 was shown to be involved in the induction of ulcerative colitis. Suppression of CCL21 expression decreased damage induced from ulcerative colitis, indicating that CCL21 targeted therapy might be an effective treatment for this disease.

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“…Commensal bacteria are required to initiate chronic intestinal inflammation in most animal models of IBD (30). The CD4 ϩ CD45RB high cell adoptive transfer model of colitis is one of the animal models of IBD that most closely reflects human IBD with respect to gene expression profiles (31). In this model of colitis, CD4 ϩ CD45RB high T cells are activated in response to commensal bacteria to initiate chronic inflammation in the absence of Tregs (32).…”

Section: Nflammatory Bowel Disease (Ibd)mentioning

confidence: 99%

The Myeloid Differentiation Factor 88 (MyD88) Is Required for CD4+ T Cell Effector Function in a Murine Model of Inflammatory Bowel Disease

Fukata¹,

Breglio²,

Chen³

et al. 2008

The Journal of Immunology

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110

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Abnormal T cell responses to commensal bacteria are involved in the pathogenesis of inflammatory bowel disease. MyD88 is an essential signal transducer for TLRs in response to the microflora. We hypothesized that TLR signaling via MyD88 was important for effector T cell responses in the intestine. TLR expression on murine T cells was examined by flow cytometry. CD4+CD45Rbhigh T cells and/or CD4+CD45RblowCD25+ regulatory T cells were isolated and adoptively transferred to RAG1−/− mice. Colitis was assessed by changes in body weight and histology score. Cytokine production was assessed by ELISA. In vitro proliferation of T cells was assessed by [3H]thymidine assay. In vivo proliferation of T cells was assessed by BrdU and CFSE labeling. CD4+CD45Rbhigh T cells expressed TLR2, TLR4, TLR9, and TLR3, and TLR ligands could act as costimulatory molecules. MyD88−/− CD4+ T cells showed decreased proliferation compared with WT CD4+ T cells both in vivo and in vitro. CD4+CD45Rbhigh T cells from MyD88−/− mice did not induce wasting disease when transferred into RAG1−/− recipients. Lamina propria CD4+ T cell expression of IL-2 and IL-17 and colonic expression of IL-6 and IL-23 were significantly lower in mice receiving MyD88−/− cells than mice receiving WT cells. In vitro, MyD88−/− T cells were blunted in their ability to secrete IL-17 but not IFN-γ. Absence of MyD88 in CD4+CD45Rbhigh cells results in defective T cell function, especially Th17 differentiation. These results suggest a role for TLR signaling by T cells in the development of inflammatory bowel disease.

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Comparative analysis of colonic gene expression of three experimental colitis models mimicking inflammatory bowel disease

Abstract: The pattern of gene expression in the CD45RB transfer model most closely reflects altered gene expression in IBD.

Cited by 141 publications

References 60 publications

Evaluation of Anti-Colitic Effect of Chung-Jang-Hwan (C-mix) in Mice

Evaluation of Anti-Colitic Effect of Chung-Jang-Hwan (C-mix) in Mice

Effect of secondary lymphoid tissue chemokine suppression on experimental ulcerative colitis in mice

The Myeloid Differentiation Factor 88 (MyD88) Is Required for CD4+ T Cell Effector Function in a Murine Model of Inflammatory Bowel Disease

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