Intestinal permeability and contractility in murine colitis

Department of Pharmacology, Erasmus University Rotterdam, The Netherlands.
Mediators of Inflammation (Impact Factor: 3.24). 02/1998; 7(3):163-8. DOI: 10.1080/09629359891090
Source: PubMed


We developed an in vitro organ bath method to measure permeability and contractility simultaneously in murine intestinal segments. To investigate whether permeability and contractility are correlated and influenced by mucosal damage owing to inflammation, BALB/c mice were exposed to a 10% dextran sulphate sodium (DSS) solution for 8 days to induce colitis. The effect of pharmacologically induced smooth muscle relaxation and contraction on permeability was tested in vitro. Regional permeability differences were observed in both control and 10% DSS-treated mice. Distal colon segments were less permeable to 3H-mannitol and 14C-PEG 400 molecules compared with proximal colon and ileum. Intestinal permeability in control vs. 10% DSS mice was not altered, although histologic inflammation score and IFN-gamma pro-inflammatory cytokine levels were significantly increased in proximal and distal colon. IL-1beta levels were enhanced in these proximal and distal segments, but not significantly different from controls. Any effect of pharmacologically induced contractility on intestinal permeability could not be observed. In conclusion, intestinal permeability and contractility are not correlated in this model of experimentally induced colitis in mice. Although simultaneous measurement in a physiological set-up is possible, this method has to be further validated.

Download full-text


Available from: Arie Van Dijk, Jan 04, 2014
  • Source
    • "The DAI value was significantly lower in rCsStefin-1-treated mice than those in DSS only-treated mice on days 7 and 8 (Fig. 1B). In cases of persistent diarrhea, the colon may be shortened, along with severe inflammation of the large intestine [30]. After the mice were sacrificed, we observed that the colon of DSS only-treated mice was shorter than the colon of rCsStefin-1 treated mice (Fig. 1C). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Many immune down-regulatory molecules have been isolated from parasites, including cystatin (cystain protease inhibitor). In a previous study, we isolated and characterized Type I cystatin (CsStefin-1) of the liver fluke, Clonorchis sinensis. To investigate whether the CsStefin-1 might be a new host immune modulator, we induced intestinal inflammation in mice by dextran sodium sulfate (DSS) and treated them with recombinant CsStefin-1 (rCsStefin-1). The disease activity index (DAI) increased in DSS only-treated mice. In contrast, the DAI value was significantly reduced in rCsStefin-1-treated mice than DSS only-treated mice. In addition, the colon length of DSS only-treated mice was shorter than that of rCsStefin-1 treated mice. The secretion levels of IFN-γ and TNF-α in the spleen and mesenteric lymph nodes (MLNs) were significantly increased by DSS treatment, but the level of TNF-α in MLNs was significantly decreased by rCsStefin-1 treatment. IL-10 production in both spleen and MLNs was significantly increased, and IL-10(+)F4/80(+) macrophage cells were significantly increased in the spleen and MLNs of rCsStefin-1 treated mice after DSS treatment. In conclusion, rCsStefin-1 could reduce the intestinal inflammation occurring after DSS treatment, these effects might be related with recruitment of IL-10 secreting macrophages.
    Full-text · Article · Sep 2011 · The Korean Journal of Parasitology
  • [Show abstract] [Hide abstract]
    ABSTRACT: In this study, we examined the relationship between the molecular weight of dextran sulfate sodium (DSS) and the features of colitis in a DSS-induced mouse model of human ulcerative colitis. DSS at three different molecular weights, 5 kD, 40 kD and 500 kD, was used in this study. DSS was administered in drinking water at 5% (w/v) to 6-7-week-old female BALB/c mice. After 7 days of treatment with DSS, the large intestine was examined histopathologically. Colitis was characterized by a loss of crypts, infiltration of inflammatory cells into the mucosa and submucosa, edema of the submucosa, erosion and ulceration and was observed in mice given the 5 kD and 40 kD forms but not the 500 kD. In the 5 kD group, colitis was observed predominantly in the cecum and upper colon. Colitis in the 40 kD group was more severe than that in the 5 kD group, and in the 40 kD group it was more severe in the lower colon than in the upper colon. These findings suggest the molecular weight of DSS to be an important factor in the murine model of colitis.
    No preview · Article · Feb 2000 · Experimental Animals
  • [Show abstract] [Hide abstract]
    ABSTRACT: A variety of mechanisms contribute to the ability of the gut to either react or remain tolerant to antigens present in the intestinal lumen. Intestinal epithelial cells can control the uptake, transmission and presentation of luminal antigens through an astonishingly diverse set of pathways. Antigens can cross the epithelial barrier via non-specific pinocytotic, specific receptor mediated, or intracellular/paracellular bypass pathways. The differential processing and presentation by a variety of restriction elements may result in the activation of functionally distinct target cell populations which have the capacity to regulate the predominant trend of immune unresponsiveness within the gut.
    No preview · Article · Jul 2001 · Seminars in Immunology
Show more