Abstract
BackgroundSalmonella 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.ResultsA 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.ConclusionsWe conclude that sseK2 is a virulence-associated gene that plays a vital role in Salmonella virulence.
Highlights
Salmonella enterica is regarded as a major public health threat worldwide
Salmonella enterica is a facultative intracellular Gramnegative pathogen that has a wide range of hosts and is regarded as a major public health concern worldwide [1]
Analysis of the ΔsseK2 mutant An in-frame deletion of the sseK2 gene was cloned into pRE112 to create a recombinant suicide plasmid
Summary
Analysis of the ΔsseK2 mutant An in-frame deletion of the sseK2 gene was cloned into pRE112 to create a recombinant suicide plasmid. Growth characteristics of the ΔsseK2 mutant The ΔsseK2 mutant, the WT strain, and a complemented strain were verified by antibiotic selection and PCR, and the results showed that their growth characteristics in LB (LuriaBertani) medium did not differ greatly (Fig. 2) This indicated that sseK2 deletion did not influence the growth characteristics of S. Typhimurium could be recovered form in the liver, spleen, and PPs. At 24 h post-infection, there was a significant difference in the number of ΔsseK2 mutant and WT bacteria recovered from the spleen, liver, and PPs. in mice infected with the complemented strain, the number of bacteria was restored to the same level as in mice infected with the WT strain (Fig. 7d, e, f). The bacterial counts from in the spleen and liver were significantly lower than those from mice infected with the parental strain 24 h, 48 h, and 72 h post-infection (P < 0.05), but the counts for the complemented strain were restored to level of the parent strain
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