Background: Salmonella actively stimulates its own uptake into the epithelial cells by inducing cytoskeleton rearrangements and membrane ruffling triggered by some proteins secreted by Salmonella into the cytosol of the epithelial cells via a type III secretion system (TTSS) encoded by genes of the Salmonella pathogenicity island 1 (SPI-1). hilA is a transcriptional activator encoded on Salmonella Pathogenicity Island 1 (SPI-1) genes.
Methods: To assess the importance of hilA in a simulation modeling of vertical infection and shedding of S. enteritidis in broiler chickens a long-term experiment was designed. Two groups of 200 fertile eggs were inoculated with 20 colony forming units (CFU) of hilA mutant of S. enteritidis or its parent strain just prior to incubation. Thirty five birds of each group were housed in separate rooms. On days 2, 4, 7, 14, 21, 28 and 35 of age, cloacal swabs from live birds as well as samples from internal organs (intestinal tract, liver and spleen) were evaluated by bacteriological or molecular methods.
Results: In most of sampling days colonization and invasion of parent strain S. enteritidis in intestine (especially ceaca) and internal organs of chickens were higher with compared to its hilA mutant but this mutant strain could still colonize in intestinal tract and even invade liver or spleen.
Conclusion: Colonization of hilA mutant of S. enteritidis indicated that hilA gene is only one part of the modulators in Salmonella invasion mechanism. The ability of hilA mutant to multiply and persist in host internal organs including ceaca may promise further research for potential of hilA mutant to prevent the initial colonization of the intestinal tract by a virulent S. enteritidis strain