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Infection and Immunity, June 2009, p. 2568-2575, Vol. 77, No. 6
0019-9567/09/$08.00+0 doi:10.1128/IAI.01537-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Kathrin Endt,
Benjamin Misselwitz,
Bärbel Stecher,
Markus Aebi,* and
Wolf-Dietrich Hardt*
Institut für Mikrobiologie, Eidgenössische Technische Hochschule, ETH Zürich, Wolfgang-Pauli-Str. 10, CH-8093 Zürich, Switzerland
Received 18 December 2008/ Returned for modification 3 February 2009/ Accepted 30 March 2009
Lipopolysaccharide (LPS) is a major constituent of the outer membrane and an important virulence factor of Salmonella enterica subspecies 1 serovar Typhimurium (serovar Typhimurium). To evaluate the role of LPS in eliciting intestinal inflammation in streptomycin-treated mice, we constructed an O-antigen-deficient serovar Typhimurium strain through deletion of the wbaP gene. The resulting strain was highly susceptible to human complement activity and the antimicrobial peptide mimic polymyxin B. Furthermore, it showed a severe defect in motility and an attenuated phenotype in a competitive mouse infection experiment, where the
wbaP strain (SKI12) was directly compared to wild-type Salmonella. Nevertheless, the
wbaP strain (SKI12) efficiently invaded HeLa cells in vitro and elicited acute intestinal inflammation in streptomycin-pretreated mice. Our experiments prove that the presence of complete LPS is not essential for in vitro invasion or for triggering acute colitis.
Published ahead of print on 13 April 2009.
Both authors contributed equally to this work.
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