Histological Analysis of Murine Colitis Induced by Dextran Sulfate Sodium of Different Molecular Weights.

Kitajima, Shuji; Takuma, Shigenobu; Morimoto, Masatoshi

doi:10.1538/expanim.49.9

Cited by 154 publications

(141 citation statements)

References 25 publications

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“…The features of colitis that we observed in CVz mice with colitis induced by 5% DSS were similar to those described in previous reports [6,21]. However, when compared to our previous data using BALB/c mice [21], the CVz IQI/Jic mice rapidly developed intestinal erosion, whereas BALB/c mice had only mild crypt loss on day three after administration of 5% DSS [13,14]. In BALB/c mice, intestinal erosion was first noticed on day five following dosage with DSS [13,14].…”

Section: Figsupporting

confidence: 90%

“…Bylund-Fellenius et al [5] have suggested that degradation of DSS by intestinal microflora is a likely reason for this difference. However, we believe that this is unlikely because in one of our previous studies we did not detect any small fragments of DSS in the feces of mice on day three after administration of 5% DSS on polyacrylamide gels [14]. Certain bacterial strains produce dextranase, which hydrolyzes the α-1, 6 glycosidic linkage [12,27].…”

Section: Figmentioning

confidence: 99%

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Dextran Sodium Sulfate-Induced Colitis in Germ-Free IQI/Jic Mice.

et al. 2001

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This study presents a histological examination of dextran sodium sulfate (DSS)-induced colitis in germ-free (GF) mice. A comparison of the pathology between GF and conventionalized mice (CVz) was made to determine the role that intestinal microflora play in DSS-induced colitis. To induce colitis, GF and CVz IQI/Jic mice were given either 5% or 1% DSS orally. Administration of 5% DSS, a common concentration used to induce colitis in mice, caused gross rectal bleeding and a marked decrease in hematocrit as early as day one in GF mice. These mice died on day three due to massive bleeding into the intestinal lumen. In contrast, CVz mice did not die during the seven-day experimental period. Histopathological examination three days after administration of 5% DSS did not reveal any colitis lesions in GF mice, but CVz mice had developed moderate colitis in the large intestine. Administration of a low concentration of DSS (1%), which only induces mild basal crypt loss in CVz mice, caused severe colitis in the distal colon in GF mice, and they died on day 14. These data suggest that intestinal microflora are not necessary for the induction of colitis. Furthermore, DSS may be highly toxic to GF mice, and when given at a concentration of 5% it causes massive bleeding into the intestinal lumen resulting in death prior to development of colitis.

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Section: Figsupporting

confidence: 90%

Section: Figmentioning

confidence: 99%

Dextran Sodium Sulfate-Induced Colitis in Germ-Free IQI/Jic Mice.

et al. 2001

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“…Thus, the DSS treatment used in our study appears to impair neurogenic responses such as spontaneous and nicotine responses without markedly changing muscular responses. The expression of molecules such as inflammatory cytokines and NO synthase induced by DSS treatment was dependent on the progress of colitis which was modulated by experimental conditions such as species including strains of mice, DSS dose and type, and treatment period (20,25,30,32). The inflammation, when severe, appeared to impair not only neuronal but also muscular functions.…”

Section: Changes Of Nicotine-induced Response In the Dsstreated Micementioning

confidence: 99%

Nicotine-Induced Neurogenic Relaxation in the Mouse Colon: Changes With Dextran Sodium Sulfate–Induced Colitis

et al. 2009

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Abstract. Nicotine has been shown to reduce both tone and muscular activity in the human colon by releasing nitric oxide (NO) from nerves. To our knowledge, however, the effect of nicotine on mouse colon has not been elucidated, and the response in tissue from ulcerative colitis (UC) has not been investigated. We examined nicotine-induced responses in colon from control mice and mice with dextran sodium sulfate (DSS)-induced UC. In controls, bath application of nicotine caused a transient relaxation in longitudinal preparations from the transverse and distal colons but not from the rectum. The response was observed in the presence of bethanechol, abolished by treatment with tetrodotoxin and hexamethonium, and mediated partially (>50%) by the NO pathway. In longitudinal preparations of the distal colon from DSStreated mice, spontaneous contractions decreased markedly, and nicotine caused contraction without relaxation in half of the preparations tested. Nicotine-induced relaxation in the presence of bethanechol was significantly decreased in the DSS-treated distal colon without changing bethanechol-induced contractions. These data suggest that 1) responses to nicotine differ dependent on colon regions, 2) DSS treatment predominantly caused nicotine-sensitive neurogenic changes in distal colon, and 3) DSS treatment may reverse the direction of nicotine-evoked responses in the colon, in mice.

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“…Colitis was induced in mice by giving 3% (wt/vol) DSS (molecular mass 30 -40 kDa; ICN Biomedicals, Aurora, OH) in drinking water ad libitum as reported by others (26,35,48). Importantly, 30-to 40-kDa DSS was utilized in this study because it is known to induce more severe colitis than 5-kDa DSS and 500-kDa DSS (25). For each mouse, weight and rectal bleeding were determined every day following the introduction of DSS.…”

Section: Synthesis Of P2281mentioning

confidence: 99%