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J Med Microbiol 57 (2008), 938-946; DOI: 10.1099/jmm.0.47848-0
© 2008 Society for General Microbiology
ISSN 1473-5644

Growth-phase regulation of lipopolysaccharide O-antigen chain length influences serum resistance in serovars of Salmonella

Denisse Bravo1, Cecilia Silva1, Javier A. Carter1, Anilei Hoare1, Sergio A. Álvarez1, Carlos J. Blondel1, Mercedes Zaldívar1, Miguel A. Valvano2 and Inés Contreras1

1 Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, PO Box 174 Correo 22, Santiago, Chile

2 Department of Microbiology and Immunology, Siebens-Drake Research Institute, University of Western Ontario, London, ON N6A 5C1, Canada

Correspondence
Inés Contreras
icontrer{at}uchile.cl

Received 26 December 2007
Accepted 11 April 2008

The amount of lipopolysaccharide (LPS) O antigen (OAg) and its chain length distribution are important factors that protect bacteria from serum complement. Salmonella enterica serovar Typhi produces LPS with long chain length distribution (L-OAg) controlled by the wzz gene, whereas serovar Typhimurium produces LPS with two OAg chain lengths: an L-OAg controlled by WzzST and a very long (VL) OAg determined by WzzfepE. This study shows that serovar Enteritidis also has a bimodal OAg distribution with two preferred OAg chain lengths similar to serovar Typhimurium. It was reported previously that OAg production by S. Typhi increases at the late exponential and stationary phases of growth. The results of this study demonstrate that increased amounts of L-OAg produced by S. Typhi grown to stationary phase confer higher levels of bacterial resistance to human serum. Production of OAg by serovars Typhimurium and Enteritidis was also under growth-phase-dependent regulation; however, while the total amount of OAg increased during growth, the VL-OAg distribution remained constant. The VL-OAg distribution was primarily responsible for complement resistance, protecting the non-typhoidal serovars from the lytic action of serum irrespective of the growth phase. As a result, the non-typhoidal species were significantly more resistant than S. Typhi to human serum. When S. Typhi was transformed with a multicopy plasmid containing the S. Typhimurium wzzfepE gene, resistance to serum increased to levels comparable to the non-typhoidal serovars. In contrast to the relevant role for high-molecular-mass OAg molecules, the presence of Vi antigen did not contribute to serum resistance of clinical isolates of serovar Typhi.

Abbreviations: L-OAg, long LPS; OAg, O antigen; VL-OAg, very long LPS.

Three supplementary figures and a supplementary table are available with the online version of this paper.






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