Hypothetical model of bacteria-mediated EGR1 induction in host epithelial cells. At the host cell surface, the bacteria may stimulate β1-integrin and/or EGFR. All strains tested exhibit absolute requirement for β1-integrin expression to trigger EGR1 induction (shown in Figure 5). Inhibition of EGFR by PD153035 blocked induction of EGR1 by all strains (shown in Figure 4). Thereby, suggesting that activation of EGFR through β1-integrin as a possible mechanism for bacteria mediated induction of EGR1. Bacterial contact with the host cells was required for the induction of EGR1 response (shown in Figure 3). Integrins and EGFR can activate several signaling molecules inside the host cell that can in turn lead to induction of EGR1. Signaling through ERK1/2 was critical for all strains, since the induction of EGR1 was blocked by ERK1/2 inhibitor (Figure 4). Also other signaling factors are partially involved in a species-dependent manner. Data suggest that H. pylori, N. gonorrhoeae and S. Enteritidis can signal through JNK to upregulate EGR1, whereas PKA is utilized only by S. Enteritidis.