This low-dose infection drives the recruitment of polymorphonuclear neutrophils (PMNs) and bacterial translocation in a PLY-dependent manner, even in absence of epithelial detachment, while other pore-forming virulence factors of the cholesterol-dependent cytolysins family, such as perfringolysin O (PFO) or intermedilysin (ILY), resulted in almost complete ablation of E-cadherin, indicating a likely pathogenetic mechanism (Xu et al., 2023). Here, CDH1 is linked to infection.