Literature DB >> 7648976

Lack of crucial role of mast cells in pathogenesis of experimental colitis in mice.

A Minocha1, C Thomas, R Omar.   

Abstract

Mast cell alterations have been implicated in the pathogenesis of chronic ulcerative colitis (UC). We studied the effect of mast cell deficiency of the severity of inflammation in a murine model of colitis. Colitis was induced in mice using dextran sodium sulfate (DSS). Mast-cell-deficient mice (WBB6F1/J-W/WV; N = 17) and normal littermates (WBB6F1/J-+/+; N = 17) were administered DSS 4% w/v for seven days, then water alone for one week, followed by 5% DSS for six days. Animals were sacrificed at the end of the protocol. Segments of proximal, mid-, and distal colon of each animal were processed for histopathological examination. Mortality and morbidity (diarrhea and weight loss) for each group were assessed. There was no significant difference between the two groups in either their clinical parameters (mortality and morbidity) or the severity of colitis as graded histopathologically. Our findings suggest that mast cells are not crucial for the development of DSS-induced colitis.

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Year:  1995        PMID: 7648976     DOI: 10.1007/bf02212698

Source DB:  PubMed          Journal:  Dig Dis Sci        ISSN: 0163-2116            Impact factor:   3.199


  41 in total

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Journal:  Dig Dis Sci       Date:  1990-11       Impact factor: 3.199

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Journal:  Dig Dis Sci       Date:  1989-09       Impact factor: 3.199

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  7 in total

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Authors:  Y Araki; A Andoh; Y Fujiyama; T Bamba
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2.  IL-33 is a crucial amplifier of innate rather than acquired immunity.

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3.  Development of colorectal sensitization is associated with increased eosinophils and mast cells in dextran sulfate sodium-treated rats.

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4.  Prevention of chronic experimental colitis induced by dextran sulphate sodium (DSS) in mice treated with FR91.

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5.  Somatostatin does not attenuate intestinal injury in dextran sodium sulphate-induced subacute colitis.

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Review 7.  The Function of the Histamine H4 Receptor in Inflammatory and Inflammation-Associated Diseases of the Gut.

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