Abstract

The role of the Salmonella Pathogenicity Islands (SPIs) in pathogenesis of Salmonella enterica Typhimurium infection in the chicken is poorly studied, while many studies have been completed in murine models. The Type VI Secretion System (T6SS) is a recently described protein secretion system in Gram-negative bacteria. The genus Salmonella contains five phylogenetically distinct T6SS encoded in differentially distributed genomic islands. S. Typhimurium harbors a T6SS encoded in SPI-6 (T6SS(SPI-6)), which contributes to the ability of Salmonella to colonize mice. On the other hand, serotype Gallinarum harbors a T6SS encoded in SPI-19 (T6SS(SPI-19)) that is required for colonization of chicks. In this work, we investigated the role of T6SS(SPI-6) in infection of chicks by S. Typhimurium. Oral infection of White Leghorn chicks showed that a Delta T6SS(SPI-6) mutant had reduced colonization of the gut and internal organs, compared with the wild-type strain. Transfer of the intact T6SS(SPI-6) gene cluster into the T6SS mutant restored bacterial colonization. In addition, our results showed that transfer of T6SS(SPI-19) from S. Gallinarum to the Delta T6SS(SPI-6) mutant of S. Typhimurium not only complemented the colonization defect but also resulted in a transient increase in the colonization of the cecum and ileum of chicks at days 1 and 3 post-infection. Our data indicates that T6SS(SPI-6) contributes to chicken colonization and suggests that both T6SS(SPI-6) and T6SS(SPI-19) perform similar functions in vivo despite belonging to different phylogenetic families.