Sigma B Contributes to Listeria monocytogenes Gastrointestinal Infection but Not to Systemic Spread in the Guinea Pig Infection Model

Abstract

ABSTRACT Contributions of the alternative sigma factor σ 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 ΔP4 inlA strain, which has a deletion in the σ B -dependent P4 inlA promoter, and the Δ 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 σ B dependent P2 prfA promoter region did not differ from that of the wild type. The virulence of the Δ sigB and ΔP4 inlA strains was attenuated in intragastrically inoculated guinea pigs, with the Δ sigB strain showing greater attenuation, while the virulence capacity of the ΔP2 prfA strain was similar to that of the wild-type strain, suggesting that attenuation of virulence due to the Δ sigB mutation does not result from loss of σ B -dependent prfA transcription. Our results show that σ B -dependent activation of inlA is important for cell invasion and gastrointestinal infection and suggest that σ B -regulated genes in addition to inlA appear to contribute to gastrointestinal infection. Interestingly, the virulence of the Δ sigB strain was not attenuated in intravenously infected guinea pigs. We conclude that (i) L. monocytogenes σ B plays a critical role in invasion of human host cells, (ii) σ B -mediated contributions to invasion are, in part, due to direct effects on inlA transcription but not on prfA transcription, and (iii) σ 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.