EGR1 is primarily activated by the EGFR–ERK1/2 pathway upon bacterial infection. Host epithelial cells were pretreated with PD153035, PD184352, SP600125, P38-IV and PKA-14:22 (inhibiting EGFR, ERK1/2, JNK, p38 and PKA, respectively) 1 h prior to infection. Bacterial infection of the host epithelial cells was carried out by co-incubation with the inhibitors for 2 h, except infection with N. gonorrhoeae that continued for 4 h. The expression of EGR1 was analyzed by qPCR. Expression of cells treated with DMSO was set to 1. (A) FaDu infected with N. meningitidis serogroup C (Nm-C). (B) FaDu infected with S. pyogenes serogroup M6 (Sp-M6). (C) AGS infected with H. pylori J99 (Hp-J99). (D) ME180 infected with N. gonorrhoea MS11 (Ng). (E) Caco-2 infected with S. Enteritidis (SE-3934). Bacteria were added to a MOI of 100 in all experiments. The white bars represent uninfected controls. The colored bars represent the infected samples. The significant difference between the infected control (DMSO) and the infected samples is marked with asterisk.