EGR1 can be upregulated by bacteria in host cells, and ERK has often been identified as a key signaling molecule in this process. The study has certain limitations imposed by the adopted experiments for adhesion assays. The bacteria were not removed after adding to the epithelial cells. Therefore, during the incubation period, the bacteria could grow and alter the composition of the medium with respect to nutrient composition and release of metabolites. The study has certain limitations imposed by the adopted experiments for adhesion assays. The bacteria were not removed after adding to the epithelial cells. Therefore, during the incubation period, the bacteria could grow and alter the composition of the medium with respect to nutrient composition and release of metabolites. However, both heat-killed and live S. Typhimurium were able to induce EGR1 at 2 h post infection (Figure 3E). Also, cell type specificity in the bacteria-mediated induction of EGR1 was observed in different cell lines (Figure 2). These observations indicated that bacteria-mediated EGR1 induction might not be due to alterations in the composition of the growth media. Instead, there is a possible role of an interaction between the bacteria and host in the bacteria-mediated induction of EGR1. Identification of the bacterial component(s) that induce EGR1 signaling and the consequences of the EGR1 induction toward bacterial pathogenicity or host defense require further investigation. The present study shows how widespread the EGR1 response is among bacteria and adds EGFR and integrin signaling as important contributors to EGR1 induction.