Abstract
Listeria monocytogenes uses a variety of transcriptional regulation strategies to adapt to the extra-host environment, the gastrointestinal tract, and the intracellular host environment. While the alternative sigma factor SigB has been proposed to be a key transcriptional regulator that facilitates L. monocytogenes adaptation to the gastrointestinal environment, the L. monocytogenes' transcriptional response to bile exposure is not well-understood. RNA-seq characterization of the bile stimulon was performed in two L. monocytogenes strains representing lineages I and II. Exposure to bile at pH 5.5 elicited a large transcriptomic response with ~16 and 23% of genes showing differential transcription in 10403S and H7858, respectively. The bile stimulon includes genes involved in motility and cell wall modification mechanisms, as well as genes in the PrfA regulon, which likely facilitate survival during the gastrointestinal stages of infection that follow bile exposure. The fact that bile exposure induced the PrfA regulon, but did not induce further upregulation of the SigB regulon (beyond that expected by exposure to pH 5.5), suggests a model where at the earlier stages of gastrointestinal infection (e.g., acid exposure in the stomach), SigB-dependent gene expression plays an important role. Subsequent exposure to bile induces the PrfA regulon, potentially priming L. monocytogenes for subsequent intracellular infection stages. Some members of the bile stimulon showed lineage- or strain-specific distribution when 27 Listeria genomes were analyzed. Even though sigB null mutants showed increased sensitivity to bile, the SigB regulon was not found to be upregulated in response to bile beyond levels expected by exposure to pH 5.5. Comparison of wildtype and corresponding ΔsigB strains newly identified 26 SigB-dependent genes, all with upstream putative SigB-dependent promoters.
Highlights
Listeria monocytogenes is a ubiquitous Gram-positive bacterium that can cause a life-threatening, invasive disease called listeriosis in humans and animals
Our data show that bile exposure at pH 5.5 elicits a broad response in L. monocytogenes, which is characterized by upregulation of motility, cell wall modification mechanisms, and the PrfA regulon
The fact that bile exposure induces the PrfA regulon, but does not seem to induce further upregulation of the SigB regulon, suggests a model where SigB-dependent gene expression is more important at an earlier stage of gastrointestinal infection than PrfA-dependent gene expression
Summary
Listeria monocytogenes is a ubiquitous Gram-positive bacterium that can cause a life-threatening, invasive disease called listeriosis in humans and animals. L. monocytogenes is the third most common cause of death from foodborne infections in the USA (Scallan et al, 2011) and has been estimated to cause over 23,000 cases of listeriosis, 23.6% of them resulting in death, each year worldwide (Maertens de Noordhout et al, 2014). The genus Listeria includes 17 species, two of which, L. monocytogenes and L. ivanovii, are considered pathogenic; L. monocytogenes has been associated with human and animal infections, while L. ivanovii has primarily been associated with animal infections (Orsi and Wiedmann, 2016). Lineage I and lineage II comprise the serotypes more commonly associated with human clinical cases, serotypes 1/2b and 4b and serotype 1/2a, respectively. In most countries and regions, lineage I is overrepresented among human isolates, while lineage II is over-represented among food isolates (Jeffers et al, 2001; Gray et al, 2004; Manuel et al, 2015), suggesting that these lineages may differ in their ecological niches and their adaptive responses to different stress conditions (Orsi et al, 2011)
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