EdC-Protein Network Formation Analysis in genetic response of human epithelial cells to SteA

Abstract

Salmonella enterica serovar Typhimurium is a gram-negative facultative anaerobic enteric pathogen in humans and animals and a leading cause of gastroenteritis. The Salmonella pathogenicity island-1(SPI-1) type III secretion system (T3SS) is critical for the invasion of host cells via the trigger mechanism by deploying a macropinocytosis-related process in enterocytes and the SPI-2 of the T3SS is responsible for the zipper mechanism and intracellular survival of Salmonella Typhimurium. These systems translocate proteins called effectors into eukaryotic host cells. SteA is one of the few Salmonella effectors that are substrates of both T3SSs. Nothing is known about the function of this protein inside the host cells. We scheduled a study to evaluate SteA gene expression in patients with Salmonella-induced gastroenteritis and natural specimens and obtained effective endocrine-disrupting chemicals (EDCs). Then, the protein-protein interaction network was constructed using the STRING database and analyzed using Cytoscape using differentially expressed genes (DEGs) with an adjusted p-value of less than 0.05. Subsequently, the network produced a PPI module. In Salmonellosis, 324 putative EDCs were discovered to influence gene regulation. The 3 genes TGFB1, CCND1, and LUM were genes that were affected by EDCs. However, these results need to be experimentally confirmed to suggest improved prevention.