Critical appraisal of the current practice in murine TNBS-induced colitis

Velde, Anje A. te; Verstege, Marleen I.; Hommes, Daniël W.

doi:10.1097/01.mib.0000227817.54969.5e

Cited by 165 publications

(151 citation statements)

References 28 publications

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“…Inflammatory events peaked at 6 h post-induction (hpi), with an increase in infiltrated neutrophils in Tg(mpx:eGFP) animals and a significant increase in mRNA expression of il1β, il8 and il10, in TNBS-exposed fishes compared with controls. These results are similar to a murine TNBS model in which an increase in neutrophilic infiltration in damaged tissue associated with a high myeloperoxidase activity [51] and an increase in TNFα levels [10] can be observed. Melanine-Concentrating Hormone (MCH) is a conserved neuropeptide involved in appetite regulation that recently has been related with intestinal inflammation [52] .…”

Section: Chemically Induced Adult Modelssupporting

confidence: 75%

“…Given the worldwide importance of these diseases, much research is currently in progress seeking answers to unresolved questions about their physiopathology, the pathways involved and new therapies to treat these conditions. Although mainly mammalian models, such as rabbits, rats and mice, are used for these studies [7][8][9][10] , other models that have been gaining ground in the field of inflammatory diseases do exist [11][12][13] . The zebrafish is a small tropical freshwater fish primarily used as a vertebrate model in developmental biology because of its characteristic high fecundity, short ex vivo development time, ease of observation in the embryonic and larval states, relative ease of genetic manipulation, and low cost of production [14] .…”

Section: Introductionmentioning

confidence: 99%

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Inflammatory diseases modelling in zebrafish

Fénero

Flores

Câmara

2016

WJEM

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The ingest of diets with high content of fats and carbohydrates, low or no physical exercise and a stressful routine are part of the everyday lifestyle of most people in the western world. These conditions are triggers for different diseases with complex interactions between the host genetics, the metabolism, the immune system and the microbiota, including inflammatory bowel diseases (IBD), obesity and diabetes. The incidence of these disorders is growing worldwide; therefore, new strategies for its study are needed. Nowadays, the majority of researches are in use of murine models for understand the genetics, physiopathology and interaction between cells and signaling pathways to find therapeutic solutions to these diseases. The zebrafish, a little tropical water fish, shares 70% of our genes and conserves anatomic and physiological characteristics, as well as metabolical pathways, with mammals, and is rising as a new complementary model for the study of metabolic and inflammatory diseases. Its high fecundity, fast development, transparency, versatility and low cost of maintenance makes the zebrafish an interesting option for new researches. In this review, we offer a discussion of the existing genetic and induced zebrafish models of two important Western diseases that have a strong inflammatory component, the IBD and the obesity. Core tip:The western lifestyle with a high fat and carbohydrates diet, lack of physical activity and stress, is a trigger for different diseases with complex interactions between the host genetics, the metabolism, the immune system and the microbiota, as the inflammatory bowel disease (IBD), obesity and diabetes. The zebrafish has 70% homology with our genes, shares anatomic and physiological characteristics with mammals, and emerges as a new model for the study of metabolic and inflammatory diseases. In this review, we examine the existing genetic and induced zebrafish models of two important Western diseases with strong inflammatory component, IBD and obesity.Morales Fénero CI, Colombo Flores AA, Câmara NOS. Inflammatory diseases modelling in zebrafish. World J Exp Med 2016; 6(1): 9-20 Available from:

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Section: Chemically Induced Adult Modelssupporting

confidence: 75%

Section: Introductionmentioning

confidence: 99%

Inflammatory diseases modelling in zebrafish

Fénero

Flores

Câmara

2016

WJEM

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“…In addition, as some clinical trials have already been performed with no description of the detailed mechanisms of the results obtained, 44,45 the data presented here are relevant in showing some strong evidence of the mucosal immune system modulation after chemotherapy and/or HSCT for inflammatory intestinal disorders. Moreover, although we did not use an established chronic IBD model with repeated TNBS injections, which induces inflammatory responses that better resemble human Crohn's disease, 21 we still observed relevant alterations in gut mucosa 2 months after the induction of inflammation and mouse treatment, suggesting that the unique TNBS enema was enough for the evaluation of the long-term effects of immunosuppression and/or HSCT in this case. However, further studies will still be performed to evaluate the role of such treatments in classical IBD models that lead to disease development closer to human chronic Crohn's disease.…”

Section: Discussionmentioning

confidence: 99%

“…21 Accordingly, in this work, our aim was to investigate the role of high-dose chemotherapy and syngenic HSCT in the treatment of intestinal inflammation and in the modulation of gut mucosal immunity in acute TNBS-induced colitis with a long-term follow-up of the disease outcome.…”

Section: Introductionmentioning

confidence: 99%

Hematopoietic SCT modulates gut inflammation in experimental inflammatory bowel disease

Godoi

Cardoso

Ferraz

et al. 2010

Bone Marrow Transplant

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Hematopoietic SCT (HSCT) and high-dose chemotherapy are being explored as therapy for various human refractory immune-mediated conditions, including inflammatory bowel diseases (IBD). Nevertheless, the exact immunological mechanisms by which the BM cells (BMCs) or immunosuppression provide remission from these diseases is not yet clear. In this work, we investigated the role of these therapies in the modulation of gut mucosal inflammation in an experimental model of IBD. Colitis was induced in mice by 2,4,6-trinitrobenzenesulfonic acid and after CY was administered (200 mg/kg) alone (CY group) or followed by BMCs infusion (HSCT group). Animals were followed for 60 days. Both HSCT and CY reduced the histopathological features of colitis significantly. Infused cells were localized in the gut, and a marked decrease of CD4 þ leukocytes in the inflammatory infiltrate on days þ 7 and þ 14 and of CD8 þ cells on day þ 7 was found in both treatments allied to impressive reduction of proinflammatory Th1 and Th17 cytokines. Although chemotherapy alone was the best treatment regarding the induction of immunosuppressive molecules, only HSCT resulted in increased survival rates compared with the control group. Our findings indicate that highdose CY followed by HSCT is effective in the modulation of mucosal immunity and in accelerating immune reconstitution after BMT, thus providing valuable tools to support the development and understanding of novel therapeutic strategies for IBD.

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“…In the TNBS-induced colitis model, which mimics Crohn's disease to a certain extent [22], DTCM-G administration significantly ameliorated colon injury according to the body weight loss, stool consistency and blood score, colon obstruction, macroscopic colon inflammation score, myeloperoxidase activity, and colon histopathology. This effect was reproducible in a murine DSS-induced colitis model that mimics human ulcerative colitis [23], wherein DTCM-G significantly ameliorated colon injury according to the body weight loss, DAI, and colon histopathology.…”

Section: Discussionmentioning

confidence: 98%

Novel anti-inflammatory agent 3-[(dodecylthiocarbonyl)-methyl]-glutarimide ameliorates murine models of inflammatory bowel disease

et al. 2015

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Objective and design To examine the effect of 3-[(dodecylthiocarbonyl)-methyl]-glutarimide (DTCM-G), a novel anti-inflammatory agent that inhibits lipopolysaccharide (LPS) -activation of RAW264.7 macrophages, on murine models of colitis and RAW264.7 cells. Materials and MethodsColitis was induced by rectally infusing trinitrobenzenesulfonic acid (TNBS) (1.5 mg in 50% ethanol) in BALB/c mice or orally administering 3% dextran sulfate sodium (DSS) for 5 days in C57BL/6 mice. The severity of colitis was assessed after intraperitoneally injecting DTCM-G (40 mg/kg). The anti-inflammatory properties of DTCM-G and its mechanisms were investigated in LPS-stimulated RAW264.7 cells.Results DTCM-G significantly ameliorated TNBS-induced colitis, according to the body weight loss, disease activity index, colonic obstruction, macroscopic colonic inflammation score, mucosal myeloperoxidase activity, and histopathology. Immunohistochemistry and isolated lamina propria mononuclear cells showed significantly reduced colonic F4/80 + and CD11b + macrophage infiltration. DTCM-G significantly suppressed tumor necrosis factor (TNF)-α and interleukin (IL)-6 messenger RNA expression in the colon, and attenuated DSS-induced colitis, according to the disease activity index and histopathology. In RAW264.7 cells, DTCM-G suppressed LPS-induced TNF-α/IL-6 production and enhanced glycogen synthase kinase-3β phosphorylation.

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Critical appraisal of the current practice in murine TNBS-induced colitis

Cited by 165 publications

References 28 publications

Inflammatory diseases modelling in zebrafish

Inflammatory diseases modelling in zebrafish

Hematopoietic SCT modulates gut inflammation in experimental inflammatory bowel disease

Novel anti-inflammatory agent 3-[(dodecylthiocarbonyl)-methyl]-glutarimide ameliorates murine models of inflammatory bowel disease

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