Interestingly, the majority of strains tested were able to upregulate EGR1 irrespective of their pathogenicity or Gram staining type (Figures 1A–D). N. meningitidis strains of different serogroups, P. aeruginosa, as well as the non-pathogenic N. lactamica and N. subflava all triggered EGR1 expression at 2 h post-inoculation (Figure 1A). A similar induction of EGR1 occurred at 2 h post-inoculation with different serogroups of S. pyogenes, S. aureus, and the non-pathogenic oral isolates L. reuteri and L. salivarius (Figure 1B). The gastric pathogen H. pylori triggered EGR1 upregulation at 2 h after infection, whereas the non-pathogenic gastric isolate L. rhamnosus did not (Figure 1C). None of the tested E. coli strains induced EGR1 in intestinal Caco-2 cells (Figure 1D). Salmonella enterica serovar Enteritidis triggered EGR1, whereas S. enterica serovar Typhimurium did not (Figure 1D). Of the cervical isolates N. gonorrhoeae, but not L. crispatus, could induce the transcription of EGR1 (Figure 1C). Western blot analysis showed that the increase in EGR1 expression also occurred at protein level (Figures 1E–H). EGR1 is an early response transcription factor that can be induced rapidly. We detected EGR1 upregulation at 1 h post-inoculation for several strains and a peak in its transcriptional activity at 2 h. Only Neisseria gonorrhoeae displayed different time kinetics with the highest EGR1 mRNA levels at 4 h after infection (Figure 1C).