The first step in bacterial pathogenesis is the colonization of the infection site through active adherence of pathogens to specific tissues. Bacterial adherence to the host epithelia generally depicts a receptor-ligand model. The bacterial adhesins act as a ligand that binds to specific receptors on the host epithelia. Colonization may not necessarily result in invasion or an inflammatory response. Host-pathogen interaction is a dynamic phenomenon; additional information about the early events that occur during host-pathogen interaction can provide new insights on bacterial virulence and pathogenicity. Although the role of EGR1 as an immediate early response factor is well established in the regulation of inflammatory and immune responses, there is limited information on whether EGR1 induction is a general response by host cells upon infection by all bacteria or a response specific for a particular bacterial strain. Also, the exact molecular pathway followed by each bacterium to induce EGR1 is not known. Therefore, the current study sought to determine whether bacterial adherence induces EGR1, whether the induction is common or specific to a selected group of bacteria, the molecular mechanisms involved and the role of EGR1 in bacterial adherence. We show that most bacteria can upregulate EGR1 in host epithelial cells, independent of the level of adherence, Gram-staining type and pathogenicity. Moreover, EGR1 upregulation is a cell type specific phenomenon, and is dependent on bacterial viability and host cell contact. Furthermore, the main pathways utilized by bacteria to trigger EGR1 expression are EGFR–ERK1/2 and β1-integrin signaling.