Histochemical study of colonic cancer in experimental colitis of rats

Tamaru, Takaji; Kobayashi, Hirofumi; Kishimoto, Seiji; Kajiyama, Goro; Shimamoto, Fumio; Brown, William R.

doi:10.1007/bf01316510

Cited by 50 publications

(29 citation statements)

References 26 publications

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“…13) Colorectal carcinomas developed in rats fed DSS for as long as 6 months. 14) Recently, Cooper et al 15) reported a relationship between the severity of DSS-induced inflammation and colorectal carcinogenesis which is similar to that of human UC-associated dysplasia and cancer regarding histopathology. However, these studies basically need a long experimental period or repeated administration of DSS.…”

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confidence: 81%

“…However, these studies basically need a long experimental period or repeated administration of DSS. [14][15][16] In addition, our previous study demonstrated that treatment with the non-genotoxic carcinogen DSS enhances the development of putative precursor lesions (aberrant crypt foci) for colonic adenocarcinoma in rats. 17) In the first report of our experimental studies of inflammation-related carcinogenesis in mouse colon, we proposed a novel mouse model, using azoxymethane (AOM) and DSS.…”

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confidence: 94%

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Sequential observations on the occurrence of preneoplastic and neoplastic lesions in mouse colon treated with azoxymethane and dextran sodium sulfate

et al. 2004

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Previously, we proposed a novel mouse model for colitis-related colon carcinogenesis using azoxymethane (AOM) and dextran sodium sulfate (DSS) (Cancer Sci 2003; 94: 965-73). In the current study, sequential analysis of pathological alterations during carcinogenesis in our model was conducted to establish the influence of inflammation caused by DSS on colon carcinogenesis in this model. Male ICR mice were given a single intraperitoneal injection of AOM (10 mg/kg body weight) and given 2% (w/v) DSS in the drinking water for 7 days, starting 1 week after the AOM injection. They were sequentially sacrificed at weeks 2, 3, 4, 5, 6, 9, 12, and 14 for histopathological and immunohistochemical examinations. Colonic adenomas were found in 2 (40% incidence and 0.40 ± ± ± ±0.49 multiplicity) of 5 mice at week 3 and colon carcinomas developed in 2 (40% incidence and 2.00 ± ± ± ±3.52 multiplicity) of 5 mice at week 4. Their incidence gradually increased with time and reached 100% (6.20 ± ± ± ±2.48 multiplicity) at week 6. At week 14, the multiplicity of adenocarcinoma was 9.75 ± ± ± ±2.49 (100% incidence). In addition, colonic dysplasia was noted at all time-points. The scores of colonic inflammation and nitrotyrosine immunohistochemistry were extremely high at early time-points and were well correlated. Our results suggest that combined treatment of mice with AOM and DSS generates neoplasms in the colonic mucosa via dysplastic lesions induced by nitrosative stress. (Cancer Sci 2004; 95: 721-727) n the developed countries, colorectal cancer (CRC) is one of the commonest non-smoking related causes of cancer deaths. Remarkable differences in the incidence worldwide have led to the hypothesis that this variation could be explained largely by environmental influences. 1)The occurrence of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is affected by several factors, including race and geography.2, 3) Life style, particularly intake of high amount of animal fat, is involved in the occurrence of IBD. 4) Over recent decades the incidence of IBD has been rising throughout the world, including Japan, as it has been in the last 50 years in Europe and North America.5) This increase may be caused by increased intake of animal fat. 6) CRC is one of the most serious complications of IBD, especially UC and CD. The risk of CRC becomes greater with increasing extent and duration of the disease. A recent meta-analysis has estimated the incidence rate at 7 per 1000 person-years duration and 12 per 1000 persons per year duration in the second and third decades of UC, respectively.7) The risk for CRC development in CD patients is also high.8) The highest risk of CRC in CD patients was reported to be 26.6 (standardized incidence ratio), although the estimate applied only to patients younger than 21 years of age. 9) Gillen et al. 10)compared the CRC risk in patients with UC and CD and found an 18-fold increase in the risk of developing CRC in extensive CD and a 19-fold increase in risk in extensive...

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confidence: 81%

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confidence: 94%

Sequential observations on the occurrence of preneoplastic and neoplastic lesions in mouse colon treated with azoxymethane and dextran sodium sulfate

et al. 2004

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“…IBD can be experimentally induced by administering dextran sulfate sodium (DSS) orally in mice (11,32), rats (37), hamsters (40), or guinea pigs (21). DSS can produce both acute and chronic ulcerative colitis, with features somewhat similar to the symptomatic and histological findings for colitis in humans (11,32).…”

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confidence: 99%

Effect of Oral Administration of Butyrivibrio fibrisolvens MDT-1 on Experimental Enterocolitis in Mice

Ohkawara

Furuya

Nagashima

et al. 2006

Clin Vaccine Immunol

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Butyrivibrio fibrisolvens MDT-1, a butyrate-producing strain, was evaluated for use as a probiotic to prevent enterocolitis. Oral administration of the MDT-1 strain (10 9 CFU/dose) alleviated the symptoms of colitis (including body weight loss, diarrhea, bloody stool, organic disorder, and mucosal damage) that are induced in mice drinking water that contains 3.0% dextran sulfate sodium. In addition, myeloperoxidase (MPO) activity levels in colonic tissue were reduced, suggesting that MDT-1 mitigates bowel inflammation. The addition of MDT-1 culture supernatant inhibited the growth of nine clinical isolates of Campylobacter jejuni and Campylobacter coli that could potentially cause enterocolitis. Infection of mice with C. coli 11580-3, one of the isolates inhibited by MDT-1 in vitro, resulted in diarrhea, mucosal damage, increased MPO activity levels in colonic tissue, increased numbers of C. coli in the cecum, and decreased body weight gain. However, administration of MDT-1 to mice, prior to and during C. coli infection, reduced these effects. These results suggest that Campylobacter-induced enterocolitis can be alleviated by using B. fibrisolvens as a probiotic.Since butyrate produced by intestinal microbiota has been implicated in protection against colon cancer and inflammatory bowel disease (IBD) (16), augmentation of butyrate production in the intestine is desirable for the maintenance of colonic health in humans and animals. We reported previously that oral administration of Butyrivibrio fibrisolvens MDT-1 (a butyrate-producing strain newly isolated from the rumen) to mice increased the rate of butyrate production by fecal microbiota and alleviated the formation of colorectal aberrant crypt foci (30). In this study, our aim was to investigate using the MDT-1 strain to alleviate the symptoms of enterocolitis, including IBD.Enterocolitis occurs frequently in humans and animals, but the pathogenesis of IBDs, including ulcerative colitis and Crohn's disease, remains unknown. Although corticosteroids and sulfasalazine are currently used commonly for the treatment of patients with IBD, the utility of these agents is limited by their adverse effects (35). In the search for new therapies for IBD, it has been reported that oral administration of Lactobacillus plantarum (23), Streptococcus salivarius (39), Escherichia coli Nissle strain 1917 (25, 33), Bifidobacterium longum (15), Lactobacillus casei Shirota (26), VSL-3 (6), and some bioactive substances (19) partially suppressed IBD.IBD can be experimentally induced by administering dextran sulfate sodium (DSS) orally in mice (11, 32), rats (37), hamsters (40), or guinea pigs (21). DSS can produce both acute and chronic ulcerative colitis, with features somewhat similar to the symptomatic and histological findings for colitis in humans (11,32). The pathogenesis of DSS-induced colitis is presently unclear, but toxic effects on colonic epithelium (12, 32), alterations of luminal bacterial flora (32, 40), and activation of macrophage inflammatory responses (31, 32) hav...

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“…The characteristics of various animal models of IBD have been extensively reviewed by Boismenu and Chen (23). The oral administration of dextran sulfate sodium (DSS) induces IBD in experimental animals including mice (24), hamsters (25), rats (26), and guinea pigs (27). Affected animals manifest weight loss, bloody diarrhea, and a hunched posture, and the histological phenotypes (24) are similar to those of human IBD.…”

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Role of γδT Cells in the Inflammatory Response of Experimental Colitis Mice

Tsuchiya

Fukuda

Hamada

et al. 2003

The Journal of Immunology

105

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We examined the severity of experimental colitis induced by dextran sulfate sodium (DSS) using immunologically manipulated mice. C57BL/6 mice showed more severe colitis than BALB/c mice, but mice of both strains recovered fully from the disease after the removal of DSS from their drinking water. The infiltrated cells at the lesions were mainly granulocytes in normal littermates. However, C.B-17 scid, IL-7Rα deficient, and TCR-Cβδ double-deficient mice showed severe colitis and did not recover from the disease even after the removal of DSS. It was found that the infiltrated cells at the lesions in the lethal strains were monocytes. Although both TCR-Cδ−/− and TCR-Cβ−/− mice showed severe colitis phenotypes, infiltration in the former is monocyte-dominant while that in the latter is granulocyte-dominant. Thus the type of cells that infiltrate at the lesions of DSS-induced experimental colitis may be controlled by functional T cell subsets. Immunohistological and RT-PCR analyses of the inflamed colon revealed that the murine homologue of human GROα released by some cells under the control of γδT cells is a possible candidate determining the severity of DSS-induced experimental colitis.

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Histochemical study of colonic cancer in experimental colitis of rats

Cited by 50 publications

References 26 publications

Sequential observations on the occurrence of preneoplastic and neoplastic lesions in mouse colon treated with azoxymethane and dextran sodium sulfate

Sequential observations on the occurrence of preneoplastic and neoplastic lesions in mouse colon treated with azoxymethane and dextran sodium sulfate

Effect of Oral Administration of Butyrivibrio fibrisolvens MDT-1 on Experimental Enterocolitis in Mice

Role of γδT Cells in the Inflammatory Response of Experimental Colitis Mice

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