| Autor: |
Grabig, A., Paclik, D., Guzy, C., Dankof, A., Baumgart, D. C., Erckenbrecht, J., Raupach, B., Sonnenborn, U., Eckert, J., Schumann, R. R., Wiedenmann, B., Dignass, A. U., Sturm, A. |
| Zdroj: |
Infection and Immunity; July 2006, Vol. 74 Issue: 7 p4075-4082, 8p |
| Abstrakt: |
ABSTRACTToll-like receptors (TLRs) are key components of the innate immune system that trigger antimicrobial host defense responses. The aim of the present study was to analyze the effects of probiotic Escherichia coliNissle strain 1917 in experimental colitis induced in TLR-2 and TLR-4 knockout mice. Colitis was induced in wild-type (wt), TLR-2 knockout, and TLR-4 knockout mice via administration of 5% dextran sodium sulfate (DSS). Mice were treated with either 0.9% NaCl or 107E. coliNissle 1917 twice daily, followed by the determination of disease activity, mucosal damage, and cytokine secretion. wt and TLR-2 knockout mice exposed to DSS developed acute colitis, whereas TLR-4 knockout mice developed significantly less inflammation. In wt mice, but not TLR-2 or TLR-4 knockout mice, E. coliNissle 1917 ameliorated colitis and decreased proinflammatory cytokine secretion. In TLR-2 knockout mice a selective reduction of gamma interferon secretion was observed after E. coliNissle 1917 treatment. In TLR-4 knockout mice, cytokine secretion was almost undetectable and not modulated by E. coliNissle 1917, indicating that TLR-4 knockout mice do not develop colitis similar to the wt mice. Coculture of E. coliNissle 1917 and human T cells increased TLR-2 and TLR-4 protein expression in T cells and increased NF-κB activity via TLR-2 and TLR-4. In conclusion, our data provide evidence that E. coliNissle 1917 ameliorates experimental induced colitis in mice via TLR-2- and TLR-4-dependent pathways. |
| Databáze: |
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