The stomach acts as a barrier against Salmonella in pigs fed a meal diet

Abstract

ORAL PRESENTATIONS Discussion: Most of the pathogenesis of salmonellosis has been described in mice, chickens and calves. Few data exist on the interactions of Salmonella with porcine phagocytes. The lack of RNI production by the porcine monocytes demonstrates that not all data collected from mice can be extrapolated to other species. In mice, the production of NO by inducible NO synthase (iNOS) is important in controlling intracellular multiplication of Salmonella bacteria (Umezawa et al., 1997). In contrast with Riber and Lind (1999), the number of intracellular bacteria steadily decreased over the 6 h period, suggesting lack of intracellular bacterial multiplication. Interestingly, opsonization with complement increased the number of surviving salmonellae. Possibly, intracellular trafficking and thus survival of the Salmonella bacteria might be influenced by entry in the host cell through complement receptor binding (Ishibashi and Arai, 1996). The production of ROS by host macrophages is an important first defence mechanism (Vazquez Torres et al., 2000), which Salmonella must circumvent in order to survive intracellularly inside the host cell. The Salmonella Typhimurium strain was able to suppress the production of ROS in porcine monocytes. This suppression was abolished when chloramphenicol treated bacteria were used, indicating that suppression of monocytic ROS production requires active bacterial protein synthesis. Individual differences between pigs were noticed both in the production of ROS and in the ability to kill Salmonella. These individual differences might account for a different course of infection, for example the development of the carrier state in some but not in other pigs.