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Lactobacillus casei prevents the development of dextran sulphate sodium-induced colitis in Toll-like receptor 4 mutant miceopen access

Authors
Chung, Yong-WooChoi, Joo-HyunOh, Tae YounEun, ChangsooHan, Dong Soo
Issue Date
Jan-2008
Publisher
BLACKWELL PUBLISHING
Keywords
dextran sulphate sodium-induced colitis; Lactobacillus casei; probiotics; Toll-like receptor 4
Citation
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, v.151, no.1, pp.182 - 189
Indexed
SCIE
SCOPUS
Journal Title
CLINICAL AND EXPERIMENTAL IMMUNOLOGY
Volume
151
Number
1
Start Page
182
End Page
189
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/172192
DOI
10.1111/j.1365-2249.2007.03549.x
ISSN
0009-9104
Abstract
Probiotics, defined as live or attenuated bacteria or bacterial products, confer a significant health benefit to the host. Recently, they have been shown to be useful in the treatment of chronic inflammatory bowel disease and infectious colitis. In this study, we investigated the effect of probiotics on the development of experimental colitis using Toll-like receptor 4 (TLR-4) mutant ((lps-/lps-) ) mice. TLR-4(lps-/lps-) and wild-type (WT) mice were given 2.5% dextran sulphate sodium (DSS) in drinking water to induce colitis with or without Lactobacillus casei pretreatment. Clinical and histological activity of DSS-colitis was attenuated markedly both in TLR-4(lps-/lps-) and WT mice pretreated with L. casei. Interestingly, histological activity was less severe in TLR-4(lps-/lps-) mice than in WT mice. The levels of myeloperoxidase activity and interleukin (IL)-12p40 were attenuated in pretreated TLR-4(lps-/lps-) mice after DSS administration. By contrast, transforming growth factor (TGF)-beta and IL-10 mRNA and protein expressions were increased markedly in pretreated TLR-4(lps-/lps-) mice. The current results suggest that L. casei has a preventive effect in the development of acute DSS-induced colitis and its action depends largely upon TLR-4 status. L. casei modulates the expression of inflammatory cytokines and down-regulates neutrophilic infiltration in the case of incomplete TLR-4 complex signalling.
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