Sus scrofa Metagenome

Salmonella enterica serovar Typhimurium is an important zoonotic gastrointestinal pathogenresponsible for food-borne disease worldwide. Studies carried out on streptomycin-treated mouse model of salmonellosis have revealed that Salmonella has developed different strategies to take advantage of the immune defenses mounted by the host. However, this approach presents a limit as antibiotic treatment modifies the intestinal microbiota precluding the full evaluation of its role during Salmonella infection. Here, in order to overcome this problem, we use a piglet model of salmonellosis to study the relationships between S. Typhimurium, the intestinal microbiota and the host. By comparing the effects induced by a wild type and an attenuated S. Typhimurium strains, we have found that there is a positive correlation between the host inflammatory response and the alterations induced in the gut microbiota community structure. The severity of modifications depends on Salmonella virulence. We have found that the attenuated znuABC mutant strain does not trigger an efficient inflammatory response and, therefore, it is outcompeted by the microbiota. In contrast, wild type S. Typhmurium induces a marked inflammation which reduces the growth of specific protecting microbiota species. In particular, we observed a reduction of butyrate-producing bacteria, that are known to provide a barrier against pathogen colonization and persistence. On the whole, our findings reveal that the magnitude of the inflammatory response is crucial to shift the balance between the protective microbiota and Salmonella.