In addition to the bacterial species described in the literature, we show that several other bacterial strains can upregulate EGR1 expression. EGR1 induction seems to be a general response of epithelial cells to bacterial colonization. In addition, we observed cell type specificity and variation in the signaling pathways used by different bacteria. Therefore, it is unlikely that EGR1 is induced by one molecule that is conserved among bacteria. Furthermore, heat killed S. Enteritidis was sufficient for EGR1 induction whereas other bacteria show requirement for viability and direct contact with the host cell. However, the role of surface molecule or bacterial component released in the supernatant upon heat treatment of S. Enteritidis needs further investigation. This result indicates a difference in the nature of bacterial EGR1 inducing factors. There are some indications in literature on the type of components could be involved, which represent a variety of molecules. For example, the type IV secretion system encoded by the Cag pathogenicity island is required for EGR1 induction by H. pylori (Keates et al., 2005). S. aureus can upregulate EGR1 through peptidoglycan (Xu et al., 2001). The molecule that is required by the bacteria also most likely depends on the host cell type. EGR1 upregulation by S. Typhimurium SL1344 and enteropathogenic E. coli in epithelial cells is dependent on their type III secretion systems (de Grado et al., 2001; Hannemann et al., 2013), whereas LPS from E. coli and Salmonella minnesota can induce EGR1 in monocytes (Coleman et al., 1992; Guha and Mackman, 2002).