Molecular and Cellular Bases of Salmonella Entry into Host Cells

Abstract

Salmonella spp. are facultative intracelluiar pathogens capable of causing disease in a great variety of animal species, including human beings (HOOK 1990). Some Salmonella serotypes are highly adapted to a specific host (e.g., S. typhi and S. gallinarum can infect only human beings and poultry, respectively) or preferentially infect one species (e.g., S. choleraesuis and S. dublin preferentially infect swine and cattle, respectively). In contrast, other serotypes can infect a broad range of hosts (e.g., S. enteritidis). The molecular bases for host adaptation are poorly understood. The type of disease caused by these microorganisms depends not only on the Salmonella serotype but also on the species and immunological status of the infected host. In human beings, the clinical manifestations of salmonellosis range from severe systemic infection to mild gastroenteritis. A common feature of the pathogenesis of all Salmonellae is their ability to gain access to cells that are normally nonphagocytic. This includes not only the cells of the intestinal epithelium, these organisms’ port of entry, but also other cells that may constitute “safe sites” for Salmonellae at later stages of their pathogenic cycle (TAKEUCHI 1967; LIN et al. 1987; CONLAN and NORTH 1992; DUNLAP et al. 1992; VERJAN et al. 1994). Although the actual mechanisms of Salmonella entry are not fully understood, work in a number of laboratories is beginning to provide some insights into this intricate process. In this chapter, the molecular and cellular bases of Salmonella entry into non-phagocytic cells will be reviewed. Most of the information available has been derived from the use of in vitro systems. However, there is enough in vivo evidence that indicates that the molecular genetic bases and mechanistic principles derived from these studies are highly relevant to the natural infection process (GALÁN and CURTISS III 1989; JONES and FALKOW 1994).