However, unlike the situation in mice, it seems that in chickens, SPI-1 genes are required for both the colonisation of the intestinal tract and the ability to reach and persist in internal organs such as the liver and spleen selleck products [17–19]. The importance of the other SPIs for Salmonella virulence in chickens is even less clear. To our knowledge, SPI-3 mutants have not been tested in chickens at all, SPI-4 mutants have been tested and shown to have no effect on chicken gut colonisation [13] and SPI-5 genes, although involved in the induction
of the proinflammatory immune response in cattle, have been described as having no significant function in chickens [13, 20]. In this study we therefore compared virulence of isogenic mutants of S. NCT-501 enterica subsp. enterica serovar Enteritidis (S. Enteritidis) defective in 5 major pathogeniCity islands for day-old chickens. To do this we deleted SPI-1 to SPI-5 from the
S. Enteritidis chromosome and orally infected chickens with these mutants. Our data indicate that the colonisation of the liver and spleen by S. Enteritidis in chickens is dependent on SPI-1 and SPI-2 and that the remaining SPIs individually have no effect on S. Enteritidis virulence although collectively they had a low effect on spleen colonisation. Results AR-13324 nmr Infection of chickens – colonisation of the caecum, liver and spleen Both on day 5 and day 12, no significant differences in caecal colonisation were observed amongst all the mutants (data not shown). When the ability to persist in internal organs was analysed, the mutants could be clustered
into 3 different groups as summarised in Table 1. The first group consisted of the wild-type strain and the ΔSPI3, ΔSPI4 and ΔSPI5 mutants. These strains colonised the liver and spleen with equal efficiency. The second group was formed by ΔSPI1-5, and the SPI3o, SPI4o and SPI5o mutants characterised by their inability to reach and persist in the liver and spleen of chickens. The last group was formed by ΔSPI1, ΔSPI2, and the SPI1o and SPI2o mutants which exhibited an intermediate tuclazepam ability to persist in liver and spleen of infected chickens (Fig. 1). Figure 1 Distribution of S . Enteritidis 147 wild-type strain and SPI mutants in the spleen of orally infected chickens. S. Enteritidis counts in the liver correlated with counts in the spleen except for the fact that ΔSPI2 mutant colonised liver significantly less efficiently than the wild type S. Enteritidis also on day 12 (not shown). Y axis, average log CFU/g of spleen ± SD. a, b – ANOVA different at p < 0.05 in comparison to the group infected with the wild-type S. Enteritidis (a) or ΔSPI1-5 mutant (b). Abbreviations: wt – wild-type S.
Related posts:
- Unlike WT mice and hnRNP F Tg mice, renal structural harm was evi
- Tumor bearing limbs of wild type mice showed a significant decrea
- Mareks Disease a CD4 T cell lymphoma of chickens caused by the Ga
- Femoral bones from OVx automobile mice exhibited reduced mRNA amo
- There was no obvious different in the growth rate of strains SC-1