Transcriptomic profiles of host epithelial cells in response to actin rearrangement induced by atypical enteropathogenic Escherichia coli

Atypical enteropathogenic Escherichia coli (aEPEC) is amongst the leading causes of diarrheal disease worldwide. The colonization of the gut mucosa by aEPEC results in actin pedestal formation at the site of bacterial attachment. This cytoskeletal rearrangement is triggered by the interaction between the bacterial adhesin intimin and its receptor Tir, which is translocated through the type three secretion system, to the host cell. While some aEPEC require tyrosine phosphorylation of Tir and recruitment of the host Nck to trigger actin polymerization, certain aEPEC strains, whose Tir is not phosphorylated, rely on the effector EspFu for efficient actin remodeling. To understand how the host responds to these different actin polymerization signaling pathways, we analyzed gene expression changes in epithelial cells infected with pedestal-forming aEPEC strains using high-throughput RNA sequencing (RNA-seq). RNA-Seq was performed on HeLa cells infected for 6 hours with aEPEC strains which trigger actin rearrangement via Tir:Nck (KOct2), Tir:EspFu (BA320) or both pathways (KOct1), as well cells infected with a strain which does not induce robust actin polymerization (KO). Uninfected cells (mock infected) were also processed as control. Each of five conditions was performed in duplicates, resulting in a total of ten samples.