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Microbiol Methods 2004,59(2):163–172.CrossRefPubMed Authors’ contributions ND and MC conceived of and participated in INK 128 manufacturer the design of the study. ND drafted the manuscript. ND, JOC, GMD and GD carried out the serotyping, AST, PFGE and VNTR. MC helped to draft the manuscript. All authors read and approved the final manuscript.”
“Background Salmonella enterica serovar Enteritidis (SE) is one of the leading etiologic agents of non-typhoid fever [1]. The disease usually manifests as a self-limiting enteritis, although systemic spread of the infections accompanied by mortalities occurs in young and immunocompromised human patients [2]. Epidemiological studies suggest that poultry flocks may serve as a major reservoir for SE organisms implicated in human clinical cases [3]. Salmonella enterica silently colonizes the intestinal and reproductive tracts of chickens, which can provide a mechanism for SE-contamination of chicken meat, shell-eggs, and hatchery eggs if proper from processing and handling are not observed [4]. Recent investigations have shown that SE utilizes its type three secretion systems (T3SS) encoded by Salmonella pathogenicity island-1 and -2 (SPI-1

and SPI-2), respectively, to promote intestinal and reproductive tract colonization [5–7]. The T3SS of Salmonellae functions as a needle-like apparatus that injects an array of effector proteins into host cells. The T3SS-1 effectors act in concert to modulate host cell cytoskeleton rearrangement, thereby facilitating bacterial entry into host epithelial cells [8]. The T3SS-2 effectors promote bacterial survival or replication within host phagocytes [9]. The T3SS effectors also shape the type of pathological changes associated with Salmonella infection via modulating host cytokine and chemokine expressions [10]. It has been commonly accepted that the outcomes of microbial infections, including salmonellosis, are largely determined by the type and magnitude of host systemic and local immune responses.