The impact of sseK2 deletion on Salmonella enterica serovar typhimurium virulence in vivo and in vitro

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 Δ sseK2 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 Δ sseK2 mutant was significantly lower than that of the WT strain. In vivo, the LD 50 (median lethal dose) of the Δ sseK2 mutant strain was increased 1.62 × 10 3 -fold compared with the WT strain. In addition, vaccinating mice with the Δ sseK2 mutant protected them against challenge with a lethal dose of the WT strain. The ability of the Δ sseK2 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 Δ sseK2 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.