Although no influence of SPIs on gut

colonisation was observed, SPI-1 and SPI-2 pathogeniCity islands were both required for S. Enteritidis colonisation of the liver and spleen, similar to previous studies [9, 13, 18, 21]. Interestingly, the decrease in counts of the ΔSPI1 and ΔSPI2 mutants in the liver and spleen was numerically not as high as that observed for single gene SPI-2 mutants in mice [22]. The importance of these two SPIs for S. Enteritidis colonisation of the liver and spleen of find more chickens was further supported by the behaviour of SPI1o and SPI2o mutants which, when compared with the ΔSPI1-5 mutant, had a significantly higher ability to colonise the spleen of infected chicken, and also by the ΔSPI1&2 selleck mutant which did not differ in colonisation of liver and spleen from the ΔSPI1-5 mutant. Interestingly, the deletion of SPI-1 resulted in a significant difference from the wild type strain liver colonisation on day 5 but not on day 12 in agreement with the results of Desin et al. [19] suggesting that decreased liver colonisation by the ΔSPI1

mutant might be caused by its slower translocation through the gut epithelium. On the other hand, the ΔSPI2 mutant showed decreased liver colonisation both on day 5 and day 12 when compared with the wild-type strain, which is consistent with the role of SPI-2 encoded proteins in intra-macrophage survival [10]. The importance of SPI-1 and SPI-2 was further confirmed by the virulence of SPI1o and SPI2o mutants because the presence of each of these pathogeniCity islands individually increased the virulence of S. Enteritidis Lenvatinib for chickens. SNX-5422 datasheet Our observations on SPI-1 and SPI-2 as the most important SPIs are similar to those of Dieye et al. except for the fact that we could not confirm that

SPI-1 would be more important than SPI-2 for Salmonella infection of chickens [17] although we did observe that SPI-1 was the most important for the induction of inflammation as supported by the cytokine inductions and the influx of heterophils. Interestingly, unlike the bovine and murine models [23, 24], we did not observe any correlation between the absence of SPI-2 and the induction of proinflammatory or any other cytokines in the avian caeca. Furthermore, we did not observe any effect of SPI-3, SPI-4 and SPI-5 deletions on the virulence of S. Enteritidis for chickens. This agrees with the observations of Morgan et al. who showed that SPI-4 genes were superfluous and SPI-3 genes and the pipB gene of SPI-5 played only a minor role in the colonisation of the chicken gut by S. Typhimurium [13]. However since the SPI1&2o mutant showed reduced ability to colonise the spleen 4 days post infection when compared with the wild-type S. Enteritidis infection, this shows that SPI-3, SPI-4 and SPI-5 collectively influenced the virulence of S. Enteritidis for chickens although these 3 SPIs individually did not contribute to the ability of S.