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Infection and Immunity, July 2006, p. 4075-4082, Vol. 74, No. 7
0019-9567/06/$08.00+0     doi:10.1128/IAI.01449-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Escherichia coli Strain Nissle 1917 Ameliorates Experimental Colitis via Toll-Like Receptor 2- and Toll-Like Receptor 4-Dependent Pathways

A. Grabig,1 D. Paclik,1 C. Guzy,1 A. Dankof,2 D. C. Baumgart,1 J. Erckenbrecht,1 B. Raupach,3 U. Sonnenborn,4 J. Eckert,5 R. R. Schumann,5 B. Wiedenmann,1 A. U. Dignass,1 and A. Sturm1*

Departments of Hepatology and Gastroenterology, Campus Virchow Klinikum,1 Pathology, Charité-Universitätsmedizin Berlin, Berlin, Germany,2 Department of Cellular Microbiology, Max Planck Institute for Infection Biology, Berlin, Germany,3 Biological Research Department, Ardeypharm GmbH, Herdecke, Germany,4 Institute of Microbiology and Hygiene, Charité-Universitätsmedizin Berlin, Berlin, Germany5

Received 5 September 2005/ Returned for modification 15 October 2005/ Accepted 15 March 2006

Toll-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 coli Nissle 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 107 E. coli Nissle 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. coli Nissle 1917 ameliorated colitis and decreased proinflammatory cytokine secretion. In TLR-2 knockout mice a selective reduction of gamma interferon secretion was observed after E. coli Nissle 1917 treatment. In TLR-4 knockout mice, cytokine secretion was almost undetectable and not modulated by E. coli Nissle 1917, indicating that TLR-4 knockout mice do not develop colitis similar to the wt mice. Coculture of E. coli Nissle 1917 and human T cells increased TLR-2 and TLR-4 protein expression in T cells and increased NF-{kappa}B activity via TLR-2 and TLR-4. In conclusion, our data provide evidence that E. coli Nissle 1917 ameliorates experimental induced colitis in mice via TLR-2- and TLR-4-dependent pathways.

* Corresponding author. Mailing address: Charité-Universitätsmedizin Berlin, Campus Virchow Clinic, Department of Hepatology and Gastroenterology, Augustenburger Platz 1, D-13353 Berlin, Germany. Phone: 49-30-450-565206. Fax: 49-30-450-553929. E-mail: andreas.sturm{at}charite.de.

Editor: J. F. Urban, Jr.

Infection and Immunity, July 2006, p. 4075-4082, Vol. 74, No. 7
0019-9567/06/$08.00+0     doi:10.1128/IAI.01449-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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