EDC-Protein network formation analysis in genetic response of human epithelial cells to SteA

Salmonella enterica serovar Typhimurium is a gram-negative facultative anaerobic enteric pathogen inhumans and animals, and a leading cause of gastroenteritis. The Salmonella pathogenicity island-۱(SPI-۱)type III secretion system (T۳SS) is critical for invasion of host cells via the trigger mechanism by deployinga macropiocytosis-related process in enterocytes and the SPI-۲ of the T۳SS is responsible for the zippermechanism and intracellular survival of Salmonella Typhimurium [۲,۳]. These systems translocate proteinscalled effectors into eukaryotic host cell. Effectors interfere with certain host signal transduction pathwaysto allow the internalization of pathogens and their survival and proliferation inside vacuoles. SteA is one ofthe few Salmonella effectors that are substrates of both T۳SSs. Nothing is known about the function of thisprotein inside the host cells.We scheduled a study to evaluate SteA gene expression in patients with Salmonella-induced gastroenteritisand natural specimens, and obtained effective endocrine disrupting chemicals (EDCs). Then, the proteinproteininteraction network was constructed using the STRING database and analyzed using Cytoscape usingdifferentially expressed genes (DEGs) with adjusted p value of less than ۰.۰۵. Subsequently, the networkproduced a PPI module. The genes in the module were then analyzed for GO and pathway enrichment. Formodule genes, EDC gene interactions were collected and reconstructed as a single EDC gene network.In Salmonellosis, ۳۲۴ putative EDCs were discovered to influence gene regulation. The ۳ genes TGFB۱,CCND۱ and LUM were genes that were affected by EDCs. However, these results need to be experimentallyconfirmed to suggest improved prevention.

کلیدواژه ها:

Salmonella enterica ، Type III secretion system ، SteA ، MicroarrayHuman epithelial cell ، Salmonella pathogenicity island