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Infection and Immunity, February 2008, p. 562-570, Vol. 76, No. 2
0019-9567/08/$08.00+0 doi:10.1128/IAI.00937-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.


Institute of Food Science and Nutrition, ETH Zurich, Schmelzbergstrasse 7, 8092 Zurich, Switzerland
Received 10 July 2007/ Returned for modification 26 August 2007/ Accepted 17 November 2007
Enterobacter sakazakii is an opportunistic pathogen that causes systemic bacteremia and meningitis with high mortality, and powdered infant formula is a frequent source of this bacterium. However, the mechanisms that this organism uses to invade and translocate through the intestinal barrier are unknown. Using Caco-2 epithelial cells, we were able to demonstrate penetration of E. sakazakii and to determine invasion-associated properties. We found that E. sakazakii entry and invasion were dependent on the exposure time and multiplicity of infection and required bacterial de novo protein synthesis but was independent of cell polarity in the presence of tight junctions. Moreover, the presence of actin filaments and microtubule structures was required, and disruption of the tight junction significantly enhanced the initial association with Caco-2 cells and the efficiency of invasion, which provides a possible explanation for the preferential occurrence of this infection in babies and neonates. This is the first description of E. sakazakii invasion of host intestinal cells, and our findings suggest that this emerging pathogen employs a novel invasion mechanism for development of systemic infection.
Published ahead of print on 10 December 2007.
Present address: Center for Agricultural Biomaterials, Seoul National University, San 56-1, Shillim-dong, Kwanak-gu, Seoul, 151-921, South Korea.
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