Illuminating the landscape of host-pathogen interactions with the bacterium Listeria monocytogenes

Abstract

Listeria monocytogenes has, in 25 y, become a model in infection biology. Through the analysis of both its saprophytic life and infectious process, new concepts in microbiology, cell biology, and pathogenesis have been discovered. This review will update our knowledge on this intracellular pathogen and highlight the most recent breakthroughs. Promising areas of investigation such as the increasingly recognized relevance for the infectious process, of RNA-mediated regulations in the bacterium, and the role of bacterially controlled posttranslational and epigenetic modifications in the host will also be discussed.

Fig. 1.

The infection by L. monocytogenes in vivo: bacteria, via contaminated food product, reach the intestinal barrier, cross it, and then disseminate to the brain and placenta (reprinted from ref. with permission from Elsevier).

Fig. 2.

The infection by L. monocytogenes in vitro. (A) The steps of the infection are schematically shown together with the bacterial factors involved and the corresponding EM images. (B) Schematic representation of the roles played by several virulence factors.

Fig. 3.

Phylogeny of the eight Listeria species. The tree depicted in continuous lines is based on nucleotide variation at 100 core genes, according to den Bakker et al. (21). The three major L. monocytogenes lineages are indicated with Roman numerals. Dotted lines indicate that the branching order and distance leading to L. rocourtiae and L. grayi, the two most distant species, are currently undefined based on this dataset (generated by S. Brisse).

Fig. 4.

Two examples of complex regulation. (A) PrfA expression regulation by an RNA thermosensor in the 5′UTR or a small RNA deriving from a SAM riboswitch (25, 38). (B) Regulation of flagella expression.

Fig. 5.

The entry of L. monocytogenes into cells. Schematic representation of the signaling pathways triggered by InlA and InlB (Top). The three bottom images show recruitment of actin, clathrin, and septin (green fluorescence) at the site of bacterial entry (bacteria shown in red).

Fig. 6.

Roles of InlA and InlB in vivo. (A) The species specificities of InlA and InlB. (B) Schematic representation of the barriers where InlA and InlB play a role in vivo. (C) Tridimensional structure of the InlA-E-cadherin and InlB-Met cocrystals (reprinted from refs. and with permission from Elsevier).