Development of dextran sulphate sodium-induced experimental colitis is suppressed in genetically mast cell-deficient <i>Ws/Ws</i> rats

Araki, Yoshio; Andoh, Akira; Fujiyama, Yoshihide; Bamba, Tadao

doi:10.1046/j.1365-2249.2000.01094.x

Cited by 76 publications

(44 citation statements)

References 30 publications

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“…As reported previously (Ahmad et al, 2000;Araki et al, 2000;Egger et al, 2000), exposing male C57BL/6J mice to DSS in the drinking water results in acute inflammation of the colon. Furthermore, in the present study we demonstrated that, as the DSS concentration increases, the severity of disease increases.…”

Section: Discussionsupporting

confidence: 71%

Novel Insights on the Effect of Nicotine in a Murine Colitis Model

AlSharari

Akbarali

Abdullah

et al. 2012

J Pharmacol Exp Ther

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Studies showed that nicotine has a positive influence on symptoms of ulcerative colitis. In the present study, we explored the effect of nicotine treatment using different routes of administration in the dextran sodium sulfate (DSS) colitis mouse model. We also investigated the effects of cotinine, a major metabolite of nicotine, in the model. C57BL6 adult male mice were given DSS solution freely in the drinking water for seven consecutive days, and tap water was given thereafter. Disease severity, length of the colon, colon tissue histology, and inflammatory markers, including colonic myeloperoxidase activity and colonic tumor necrosis factor-a levels, were evaluated. The effect of nicotine and cotinine treatments via various different routes of administration were examined the DSS model. In addition, we measured the plasma levels of nicotine and cotinine in our treatment protocols. Administration of low, but not high, doses of oral nicotine in DSS-treated mice resulted in a significant decrease in disease severity, histologic damage scores, as well as colonic level of tumor necrosis factor-a. However, the anti-inflammatory effect of nicotine was not seen after chronic s.c. or minipump infusion of the drug. Differences in plasma levels of nicotine and cotinine do not seem to account for this lack of effect. Finally, oral cotinine alone failed to show a significant effect in the DSS model of colitis. These results highlight that dose and route of administration play a critical role in the protective effect of nicotine in the DSS mouse colitis model.

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Section: Discussionsupporting

confidence: 71%

Novel Insights on the Effect of Nicotine in a Murine Colitis Model

AlSharari

Akbarali

Abdullah

et al. 2012

J Pharmacol Exp Ther

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“…For example, studies in genetically mast cell-deficient mice have shown that mast cells can enhance the development and͞or magnitude of certain T cell-associated responses. These responses include those elicited by exogenous antigens (Ags), such as in models of contact hypersensitivity (CHS) (3)(4)(5), delayedtype hypersensitivity (6), and asthma (7,8), and in models of autoimmune diseases, such as experimental autoimmune encephalomyelitis (9), Ab-induced arthritis (10), and inflammatory bowel disease (11). Moreover, in some of these settings, including models of asthma or CHS, mast cell activation may reflect, at least in part, the recognition of specific Ags by IgE (7,8,12) or IgG1 (7,8,10,13) Abs bound to FcRI or Fc␥RIII receptors on the mast cell surface.…”

mentioning

confidence: 99%

Mast cells enhance T cell activation: Importance of mast cell-derived TNF

Nakae

Suto

Kakurai

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

228

209

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Mast cells are not only important effector cells in immediate hypersensitivity reactions and immune responses to pathogens but also can contribute to T cell-mediated disorders. However, the mechanisms by which mast cells might influence T cells in such settings are not fully understood. We find that mast cells can enhance proliferation and cytokine production in multiple T cell subsets. Mast cell-dependent enhancement of T cell activation can be promoted by FcRI-dependent mast cell activation, TNF production by both mast cells and T cells, and mast cell-T cell contact. However, at high concentrations of cells, mast cells can promote T cell activation independent of IgE or TNF. Finally, mast cells also can promote T cell activation by means of soluble factors. These findings identify multiple mechanisms by which mast cells can influence T cell proliferation and cytokine production.allergy ͉ asthma ͉ autoimmunity ͉ cytokines ͉ immune response

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“…Iba et al (2002) reported that mast cell numbers in the rectum were significantly increased after DSS treatment in rats. In mast cell-deficient mice, macroscopic colonic damage was significantly suppressed compared with control mice after DSS treatment (Araki et al, 2000). Chymase is located in mast cell granules, and the mechanisms underlying reduced colonic damage in mast cell-deficient mice may include suppression of chymase levels.…”

Section: Discussionmentioning

confidence: 93%

Role of Chymase-Dependent Matrix Metalloproteinase-9 Activation in Mice with Dextran Sodium Sulfate-Induced Colitis

Ishida

Takai²,

Murano³

et al. 2007

J Pharmacol Exp Ther

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Matrix metalloproteinase (MMP)-9 plays an important role in the pathogenesis of colitis. Recent studies have demonstrated that chymase is involved in the conversion of promatrix metalloproteinase (proMMP)-9 to MMP-9. However, whether chymase contributes to the activation of proMMP-9 in colitis has remained unclear. In this study, we administered 5% dextran sodium sulfate (DSS) solution to mice for 7 days. At 7 days after starting administration, both chymase activity and MMP-9 activity were significantly increased. In extract from colitis in DSS-treated mice, MMP-9 activity was significantly increased after 8 h of incubation, but increased activity was almost completely suppressed in the presence of a chymase inhibitor, 2-(5-formylamino-6-oxo-2-phenyl-1,6-dihydropyrimidine-1-yl)-N-[{3,4-dioxo-1-phenyl-7-(2-pyridyloxy)}-2-heptyl] acetamide (NK3201). At 7 days after starting administration, intestinal length was significantly shorter in DSStreated mice than in normal mice, but these changes were significantly prevented by NK3201 (10 mg/kg per day i.p.). Disease activity index and histological damage score were also significantly reduced by NK3201. The filtrated neutrophil number was significantly decreased by NK3201. Furthermore, NK3201 significantly attenuated not only chymase activity but also MMP-9 activity in DSS-treated mice. These findings suggest that chymase plays an important role in the development of colitis via MMP-9 activation.Ulcerative colitis is an inflammatory bowel disease (IBD) affecting the distal colon; the etiology remains unclear. In chronic tissues of patients with IBD, the synthesis and release of inflammatory cytokines and recruitment of inflammatory cells induce the degradation of extracellular matrix (ECM). Matrix metalloproteinases (MMPs) are important enzymes for degrading ECM proteins, and MMPs are reportedly involved in the pathogenesis of IBD via ECM degradation . MMPs are a family of zinc-and calcium-dependent endopeptidases. Among the MMPs, MMP-2 and MMP-9 are known as gelatinases and are consistently up-regulated during active flares of IBD in patients and animal models of colitis (Baugh et al., 1999;Tarlton et al., 2000). In particular, MMP-9 may play an important role in the degradation of ECM in ulcerative colitis. Oral administration of dextran sodium sulfate (DSS) is used to induce colitis in animal models, and the resulting colonic lesions resemble those observed in patients with ulcerative colitis (Elson et al., 1995). DSS-induced colitis is significantly attenuated in MMP-9-deficient mice but not in MMP-2-deficient mice (Castaneda et al., 2005;Garg et al., 2006). Thus, MMP-9 inhibition might offer a useful strategy for attenuating the development of colitis.Chymase is a chymotrypsin-like serine protease located in the secretory granules of mast cells. Serine proteases, such as MMP-3, and trypsin are known to process promatrix metalloproteinase (proMMP)-9 to MMP-9 in vitro (Sang et al., 1995;Shapiro et al., 1995). Fang et al. (1996Fang et al. ( , 1997 reported tha...

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Development of dextran sulphate sodium-induced experimental colitis is suppressed in genetically mast cell-deficient Ws/Ws rats

Cited by 76 publications

References 30 publications

Novel Insights on the Effect of Nicotine in a Murine Colitis Model

Novel Insights on the Effect of Nicotine in a Murine Colitis Model

Mast cells enhance T cell activation: Importance of mast cell-derived TNF

Role of Chymase-Dependent Matrix Metalloproteinase-9 Activation in Mice with Dextran Sodium Sulfate-Induced Colitis

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