This has been reported previously in mice where the deletion of the entire SPI1 had a different effect than a single gene deletion [33]. However, it seems unlikely as other studies have yielded results that are consistent with some of our findings. For instance, two studies that screened transposon mutant libraries of Typhimurium for

reduced colonization of the chicken gastrointestinal tract either found mutations in SPI1 but not in SPI2 [28] or that SPI1 mutations had greater influence [29]. Despite the fact that cecal swabbing was used to recover strains in these two studies, which may fail Selleckchem Smoothened Agonist to catch low level colonization, both studies still identified SPI1 as important in intestinal colonization.

Cecal colonization was also reported to decrease substantially after the deletion of SPI1 T3SS components [26]. Additionally, a study with S. enterica serovar Enteritidis, which displays an infection pattern similar to MAPK inhibitor Typhimurium, showed that deletion of the ssrA gene, encoding the sensor component of the SsrAB two-component system that is the major regulator of the SPI2 gene expression, did not affect the colonization of the chicken digestive tract [34]. All together these results suggest that Typhimurium relies less on SPI2 than on SPI1 for colonization of the intestinal track in one-week-old chicks. In contrast, Jones et al. [27] analyzed the contribution of SPI1 and SPI2 to the colonization of chickens by Typhimurium through the deletion of a single T3SS structural gene in each. They concluded that the SPI2 T3SS was required for systemic infection and played a significant role in the colonization of the

gastrointestinal tract, while the SPI1 T3SS was involved in both compartments without being essential [27]. There are several important differences between that study and ours. First, Jones et al. used derivatives of the Typhimurium F98 strain [9] while we used derivatives of the UK-1 strain [36]. While both have been well characterized for virulence and persistence in chickens, their mean lethal dose (LD50) in day of hatch chicks differ by two orders of magnitude with F98 at 5 × 105 cfu [35] and UK-1 at approximately 2 × 103 [36]. Second, they studied mutants this website in which a single structural T3SS gene was inactivated while in our mutants the entire SPI1 and all the SPI2 T3SS structural genes were deleted. Third, they determined the level of colonization of the chicken by calculating the bacterial density (number of colony forming unit per gram) in the organs after administration of single strains while we infected the chickens with mixtures of the two strains being compared and determined the competitive index. These differences may account for the differences in the results.