Salmonella is a foodborne pathogen that causes enterogastritis among humans, livestock and poultry, and it not only causes huge economic losses for the feed industry but also endangers public health around the world. However, the prevention and treatment of Salmonella infection has remained poorly developed because of its antibiotic resistance. Bacterial quorum sensing (QS) system is an intercellular cell–cell communication mechanism involving multiple cellular processes, especially bacterial virulence, such as biofilm formation, motility, adherence, and invasion. Therefore, blocking the QS system may be a new strategy for Salmonella infection independent of antibiotic treatment. Here, we have reviewed the central role of the QS system in virulence regulation of Salmonella and summarized the most recent advances about quorum quenching (QQ) in virulence attenuation during Salmonella infection. Unraveling the complex relationship between QS and bacterial virulence may provide new insight into the therapy of pathogen infection.

Salmonella enterica is regarded as a major public health threat worldwide. Salmonella secretes the novel translocated effector protein K2 (SseK2), but it is unclear whether this protein plays a significant role in Salmonella enterica Typhimurium virulence. A ΔsseK2 mutant of S. Typhimurium exhibited similar growth curves, adhesion and invasive ability compared with wild-type (WT) bacteria. However, deletion of sseK2 rendered Salmonella deficient in biofilm formation and the early proliferative capacity of the ΔsseK2 mutant was significantly lower than that of the WT strain. In vivo, the LD50 (median lethal dose) of the ΔsseK2 mutant strain was increased 1.62 × 103-fold compared with the WT strain. In addition, vaccinating mice with the ΔsseK2 mutant protected them against challenge with a lethal dose of the WT strain. The ability of the ΔsseK2 mutant strain to induce systemic infection was highly attenuated compared with the WT strain, and the bacterial load in the animals’ internal organs was lower when they were infected with the ΔsseK2 mutant strain than when they were infected with the WT strain. We conclude that sseK2 is a virulence-associated gene that plays a vital role in Salmonella virulence.