Adult mice were treated with dextran sulfate sodium (DSS)
and infected with Citrobacter rodentium for developing a
novel murine colitis model. C57BL/6N mice (7-week-old)
were divided into four groups. Each group composed of control,
dextran sodium sulfate-treated (DSS), C. rodentiuminfected
(CT), and DSS-treated and C. rodentium-infected
(DSS-CT) mice. The DSS group was administered 1% DSS
in drinking water for 7 days. The CT group was supplied
with normal drinking water for 7 days and subsequently infected
with C. rodentium via oral gavage. The DSS-CT group
was supplied with 1% DSS in drinking water for 7 days and
subsequently infected with C. rodentium via oral gavage. The
mice were sacrificed 10 days after the induction of C. rodentium
infection. The DSS-CT group displayed significantly
shorter colon length, higher spleen to body weight ratio, and
higher histopathological score compared to the other three
groups. The mRNA expression levels of tumor necrosis factor
(TNF)-α and interferon (INF)-γ were significantly upregulated;
however, those of interleukin (IL)-6 and IL-10 were
significantly downregulated in the DSS-CT group than in
the control group. These results demonstrated that a combination
of low DSS concentration (1%) and C. rodentium
infection could effectively induce inflammatory bowel disease
(IBD) in mice. This may potentially be used as a novel
IBD model, in which colitis is induced in mice by the combination
of a chemical and a pathogen.
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Some species of lactic acid bacteria have been shown to be beneficial in inflammatory bowel disease (IBD). In the pre-sent study, a strain of lactic acid bacterium (Lactobacillus paracasei LS2) was isolated from the Korean food, kimchi, and was shown to inhibit the development of experimental colitis induced by dextran sulfate sodium (DSS). To inves-tigate the role of LS2 in IBD, mice were fed DSS in drinking water for seven days along with LS2 bacteria which were administered intragastrically to some of the mice, while phos-phate-buffered saline (PBS) was administered to others (the controls). The administration of LS2 reduced body weight loss and increased survival, and disease activity indexes (DAI) and histological scores indicated that the severity of colitis was significantly reduced. The production of inflammatory cy-tokines and myeloperoxidase (MPO) activity also decreased. Flow cytometry analysis showed that the number of Th1 (IFN-γ) population cells was significantly reduced in the LS2- administered mice compared with the controls. The admini-stration of LS2 induced the increase of CD4+FOXP3+ Treg cells, which are responsible for IL-10. Numbers of macro-phages (CD11b+ F4/80+), and neutrophils (CD11b+ Gr-1+) among lamina propria lymphocytes (LPL) were also reduced. These results indicate that LS2 has an anti-inflammatory effect and ameliorates DSS-induced colitis.
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