Molecular Basis of the Interaction ofSalmonellawith the Intestinal Mucosa

Abstract

SUMMARY Salmonella is one of the most extensively characterized bacterial pathogens and is a leading cause of bacterial gastroenteritis. Despite this, we are only just beginning to understand at a molecular level how Salmonella interacts with its mammalian hosts to cause disease. Studies during the past decade on the genetic basis of virulence of Salmonella have significantly advanced our understanding of the molecular basis of the host-pathogen interaction, yet many questions remain. In this review, we focus on the interaction of enterocolitis-causing salmonellae with the intestinal mucosa, since this is the initiating step for most infections caused by Salmonella. Animal and in vitro cell culture models for the interaction of these bacteria with the intestinal epithelium are reviewed, along with the bacterial genes that are thought to affect this interaction. Lastly, recent studies on the response of epithelial cells to Salmonella infection and how this might promote diarrhea are discussed.

Characterization of a porcine intestinal epithelial cell line for in vitro studies of microbial pathogenesis in swine

“…are facultative intracellular pathogens and the infection process of epithelial cells is characterized by initial attachment/adhesion followed by invasion and formation of an intracellular Salmonella-containing vacuole in which the pathogen replicates. This process involves both Salmonella-encoded proteins and cytoskeletal recruitment and rearrangements by the host cells (Darwin and Miller 1999). As shown in Fig.…”

“…The infection of the intestinal epithelia comprises different mechanisms including attachment and/or invasion of bacteria to the cells, proliferation of the pathogens and host cell responses (Darwin and Miller 1999;Bavoil et al 2000;Carlson et al 2002).…”

Virulent strains of Salmonella enteritidis disrupt the epithelial barrier of Caco-2 and HEp-2 cells

“…This is possibly due to the necessity of the bacteria to enter the cell by a process regulated by the epithelial cell. From these studies, it is probable that these two distinct species of Salmonella have unique mechanisms of interaction with intestinal epithelial cells (Bourdet-Sicard, and Tran Van Nhieu 1999; Darwin and Miller 1999;Kops et al 1997).…”

“…The release of LDH into the supernatant of the cell culture by the high-virulence strains of S. enteritidis could be due to the local disruption of cytoplasm, with blebs protruding from the apical surface, a process observed after S. typhimurium infection (Bourdet-Sicard, and Tran Van Nhieu 1999; Darwin and Miller 1999;Gahring et al 1990). Furthermore, the results obtained in our study using light microscopy revealed that, although the highly virulent S. enteritidis 3934 strain did not produce striking damage to the epithelial cells, spaces between tight junctions could be observed, suggesting a possible entrance between cells.…”

Animal Feed Production and Contamination by Foodborne Salmonella

“…Salmonella and other foodborne pathogens become virulent when exposed to different stress factors such as non-optimal pH, oxygen availability, and osmolarity (Mekalanos, 1992;Foster and Spector, 1995;Bajaj et al, 1996). In addition to the synthesis of toxins and survival factors, virulence is expressed via production of a variety of attachment and invasion proteins that interact with the intestinal cells (Darwin and Miller, 1999). It is conceivable that Salmonella is suffi ciently exposed to a number of byproducts from different production aspects both in feed and food product manufacture, where virulent activity could be activated.…”