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Infection and Immunity, February 2006, p. 876-886, Vol. 74, No. 2
0019-9567/06/$08.00+0 doi:10.1128/IAI.74.2.876-886.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Sigma B Contributes to Listeria monocytogenes Gastrointestinal Infection but Not to Systemic Spread in the Guinea Pig Infection Model
M. R. Garner,1
B. L. Njaa,2
M. Wiedmann,1 and
K. J. Boor1*
Department of Food Science,1
Department of Biomedical Sciences, Cornell University, Ithaca, New York 148532
Received 19 August 2005/
Returned for modification 29 September 2005/
Accepted 8 November 2005
Contributions of the alternative sigma factor
B to Listeria monocytogenes infection were investigated using strains bearing null mutations in sigB, prfA, or inlA or in selected inlA or prfA promoter regions. The
P4inlA strain, which has a deletion in the
B-dependent P4inlA promoter, and the
sigB strain had significantly reduced invasion efficiencies relative to that of the wild-type strain in the Caco-2 human colorectal epithelial cell line, while the invasion efficiency of a strain bearing a deletion in the partially
B dependent P2prfA promoter region did not differ from that of the wild type. The virulence of the
sigB and
P4inlA strains was attenuated in intragastrically inoculated guinea pigs, with the
sigB strain showing greater attenuation, while the virulence capacity of the
P2prfA strain was similar to that of the wild-type strain, suggesting that attenuation of virulence due to the
sigB mutation does not result from loss of
B-dependent prfA transcription. Our results show that
B-dependent activation of inlA is important for cell invasion and gastrointestinal infection and suggest that
B-regulated genes in addition to inlA appear to contribute to gastrointestinal infection. Interestingly, the virulence of the
sigB strain was not attenuated in intravenously infected guinea pigs. We conclude that (i) L. monocytogenes
B plays a critical role in invasion of human host cells, (ii)
B-mediated contributions to invasion are, in part, due to direct effects on inlA transcription but not on prfA transcription, and (iii)
B plays a critical role during the gastrointestinal stage of listeriosis in the guinea pig but is not important for systemic spread of the organism.
* Corresponding author. Mailing address: Department of Food Science, 413 Stocking Hall, Cornell University, Ithaca, NY 14853. Phone: (607) 255-3111. Fax: (607) 254-4868. E-mail:
kjb4{at}cornell.edu.
Editor: J. T. Barbieri
Infection and Immunity, February 2006, p. 876-886, Vol. 74, No. 2
0019-9567/06/$08.00+0 doi:10.1128/IAI.74.2.876-886.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
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