Abstract
During infection, the foodborne bacterial pathogen Listeria monocytogenes dynamically influences the gene expression profile of host cells. Infection-induced transcriptional changes are a typical feature of the host-response to bacteria and contribute to the activation of protective genes such as inflammatory cytokines. However, by using specialized virulence factors, bacterial pathogens can target signaling pathways, transcription factors, and epigenetic mechanisms to alter host gene expression, thereby reprogramming the response to infection. Therefore, the transcriptional profile that is established in the host is delicately balanced between antibacterial responses and pathogenesis, where any change in host gene expression might significantly influence the outcome of infection. In this review, we discuss the known transcriptional and epigenetic processes that are engaged during Listeria monocytogenes infection, the virulence factors that can remodel them, and the impact these processes have on the outcome of infection.
Highlights
Regulation of gene expression at the transcriptional level is fundamental in enabling a cell to enact transient or permanent phenotypic changes
Key Contribution: In this review we provide a global view of the host transcriptional response to Listeria monocytogenes infection and the mechanisms used by the pathogen to alter gene expression to its own advantage
Transcriptional responses to Listeria monocytogenes (Lm) infection include the induction of two broad categories of gene expression profiles: one dominated by nuclear factor-κB (NF-κB) and Mitogen-activated protein kinase (MAPK)-regulated inflammatory genes; and another composed of interferon-stimulated genes (ISGs) [24,29,35]
Summary
Regulation of gene expression at the transcriptional level is fundamental in enabling a cell to enact transient or permanent phenotypic changes. Certain repressive histone marks recruit proteins such as heterochromatin protein 1 (HP1), which holds chromatin in its condensed and silent configuration, and has more stable, long lasting effects [7,16,17] Gene regulators, such as transcription factors and epigenetic processes, work concurrently to ensure appropriate and robust transcriptional regulation in response to environmental stimuli and stress, such as bacteria. Lm is detected by multiple families of pattern recognition receptor (PRR), including the nucleotide-binding domain and leucine-rich repeat (NLR) proteins, and toll-like receptors (TLRs), which respectively localize to the cytoplasm and cellular membranes These receptors play a crucial role in generating the transcriptional response to Lm by signaling to transcription factors such as nuclear factor-κB (NF-κB) [26], which regulates the expression of hundreds of genes important for inflammatory and immune responses [27,28,29]. We will focus on the transcriptional and epigenetic changes that arise upon sensing Lm during infection, the mechanisms used by Lm to influence these events, and how these illustrate the complex signaling crosstalk that takes place during infection
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