Listeria monocytogenes: survival and adaptation in the gastrointestinal tract

Abstract

The foodborne pathogen Listeria monocytogenes has the capacity to survive and grow in a diverse range of natural environments. The transition from a food environment to the gastrointestinal tract begins a process of adaptation that may culminate in invasive systemic disease. Here we describe recent advances in our understanding of how L. monocytogenes adapts to the gastrointestinal environment prior to initiating systemic infection. We will discuss mechanisms used by the pathogen to survive encounters with acidic environments (which include the glutamate decarboxylase and arginine deiminase systems), and those which enable the organism to cope with bile acids (including bile salt hydrolase) and competition with the resident microbiota. An increased understanding of how the pathogen survives in this environment is likely to inform the future design of novel prophylactic approaches that exploit specific pharmabiotics; including probiotics, prebiotics, or phages.

Keywords: Listeria; acid; bile; gastrointestinal; infection; pathogenesis; stress; virulence.

Figure 1

Two major acid tolerance mechanisms in L. monocytogenes. The GAD system is proposed to function through the import of glutamate into the cell (via GadT1 or GadT2) which is converted to GABA via Gad enzymes (GadD1, D2, or D3) in the cytoplasm. The GABA is then thought to be exported from the cell by means of the antiport systems (GadT1/T2). The consumption of protons during the reaction is contributes to the reduction in intracellular hydrogen ion concentration (Cotter et al., 2001). Karatzas et al. (2012) have recently proposed the existence of an intracellular GAD_i system that operates in the absence of added glutamate. The ADI system has also been proposed to operate via utilization of intracellular arginine as well as via arginine import (Ryan et al., 2009). The arginine biosynthetic pathway is shown. Black arrows indicate genes that are upregulated during growth of Listeria in the GI tract of germ-free mice and further upregulated through in situ exposure to Lactobacillus spp. (Archambaud et al., 2012). In such cases the enzyme is highlighted with an asterisk.