Next, we aimed to identify the molecular mechanisms through which bacteria induce EGR1. There are several signaling pathways upstream of EGR1 and therefore we used different chemical inhibitors to specifically block each of these pathways. Interestingly, inhibition of ERK1/2 and EGFR completely abolished the EGR1 upregulation for all the 5 strains tested (Figures 4A–E). Inhibition of signaling through JNK reduced EGR1 upregulation for H. pylori, N. gonorrhoeae and S. Enteritidis (Figures 4C–E). Inhibition of PKA resulted in a reduction of EGR1 induction specifically for S. Enteritidis (Figure 4E). P38 pathway played no role in the bacteria mediated induction of EGR1. Treatment of the host cells with the inhibitors did not affect the adhesion of the bacteria, indicating that EGR1 upregulation is not important for bacterial attachment to host cells (Supplementary Figure S3 online). Since, the blocking of EGFR and ERK1/2 exhibited the strongest inhibition of EGR1 upregulation for all the bacteria tested, we propose that the EGFR–ERK1/2 signaling pathway is a commonly used route for bacterial induction of EGR1.