Abstract
Listeria monocytogenes strains are classified in at least three distinct phylogenetic lineages. There are correlations between lineage classification and source of bacterial isolation; e.g., human clinical and food isolates usually are classified in either lineage I or II. However, human clinical isolates are overrepresented in lineage I, while food isolates are overrepresented in lineage II. sigma(B), a transcriptional regulator previously demonstrated to contribute to environmental stress responses and virulence in L. monocytogenes lineage II strains, was hypothesized to provide differential abilities for L. monocytogenes survival in various niches (e.g., food and human clinical niches). To determine if the contributions of sigma(B) to stress response and virulence differ across diverse L. monocytogenes strains, DeltasigB mutations were created in strains belonging to lineages I, II, IIIA, and IIIB. Paired parent and DeltasigB mutant strains were tested for survival under acid and oxidative stress conditions, Caco-2 cell invasion efficiency, and virulence using the guinea pig listeriosis infection model. Parent and DeltasigB mutant strain transcriptomes were compared using whole-genome expression microarrays. sigma(B) contributed to virulence in each strain. However, while sigma(B) contributed significantly to survival under acid and oxidative stress conditions and Caco-2 cell invasion in lineage I, II, and IIIB strains, the contributions of sigma(B) were not significant for these phenotypes in the lineage IIIA strain. A core set of 63 genes was positively regulated by sigma(B) in all four strains; different total numbers of genes were positively regulated by sigma(B) in the strains. Our results suggest that sigma(B) universally contributes to L. monocytogenes virulence but specific sigma(B)-regulated stress response phenotypes vary among strains.