Growth factor receptors can cooperate with integrins to induce signaling and/or enhance the response upon activation by their ligands (Giancotti and Tarone, 2003). Integrin and EGFR cross-talk has also been implicated in EGR1 expression (Cabodi et al., 2009). We therefore used siRNA to silence β1-integrins and integrin-linked kinase (ILK) in host epithelial cells to investigate whether integrin signaling is involved in EGR1 upregulation by bacteria. Silencing β1-integrins completely inhibited the induction of EGR1 expression after infection with N. meningitidis, S. pyogenes, H. pylori, N. gonorrhoeae, and S. Enteritidis (Figures 5A–E). ILK played role in the upregulation of EGR1 only for S. Enteritidis (Figure 5E). The adherence level of bacteria to host cells was not affected by silencing of EGR1, β1-integrins or ILK (Supplementary Figure S4). Downregulation of the transcription of the target genes by siRNA treatment in each cell line was confirmed using qPCR (Supplementary Figure S5). Therefore, signaling through integrins is important for bacteria-mediated EGR1 induction.